Showing posts with label treatment. Show all posts
Showing posts with label treatment. Show all posts
Friday, November 12, 2010
ENTAMOEBA HISTOLYTICA
Microbiology
Enteric protozoan
Cyst: 5-20 micrometer with one to four nuclei
Trophozoite (ameba): 12-60 micrometer with a single nucleus, a centrally located nucleolus with a uniformly distributed peripheral chromatin
Many strains, differentiated by isoenzyme analysis
Epidemiology
10% of the world is infected
50,000-100,000 E. histolytica-associated deaths per year (third leading parasitic cause of death in the world)
Endemic in Mexico, India, West and South Africa and portions of Central and South America
Vast majority (90%) of patients remain asymptomatic
High risk factors for invasive diseases in North America:
recent immigration, institutionalization and homosexuality
Transmission by fecal-oral route
Clinical syndromes
Intestinal:
Asymptomatic colonization
Acute amebic colitis
Fulminant colitis
Ameboma
Extraintestinal
Hepatic abscess
Pleuropulmonary
Peritonea
Pericardial
brain abscesses
Diagnosis
Serology (generally positive after 7 days)
Cyst and parasite in stool (rapid examination after special coloration: modify Kinouyn: as trophozoites die rapidly)
Comments on treatment
Surgical drainage if abscess
Asymptomatic cyst passer:
recommended: Paromomycin or Iodoquinol
alternative: diloxanide furoate
Diarrhea
recommended: Metronidazole and (Paromomycin or Iodoquinol)
alternative: (tinidazol or ornidazole) and (Paromomycin or Iodoquinol)
Extraintestinal infection:
Metronidazole and Iodoquinol
HELICOBACTER PYLORI AND PEPTIC ULCER
Microbiology
Formerly Campylobacter pylori
Spiral-shaped gram-negative bacillus
Ability to survive the acidic pH of gastric fluids
Epidemiology
Implicated as a cause of duodenal and gastric ulcers
Infection increasing with age
Natural reservoir in humans
Transmission is fecal-oral
Clinical syndromes
Duodenal and gastric ulcers
Dyspepsia (non-ulcer)
Gastric carcinoma
Diagnosis
Urease test (breath test)
Culture
Gastric biopsy
Serology
Comments on treatment
Susceptible in vitro to a variety of antimicrobial agents: Tetracycline, Metronidazole, Amoxicillin and Clarithromycin
Resistance to these antibiotics has been described (associated with treatment failures)
Recommended: see Ulcer, Gastric & Duodenal for more details
Amoxicillin and Clarithromycin and (omeprazole or lansoprazole)
Alternative:
bismuth and Tetracycline and Metronidazole and omeprazole
Hepatitis-B
Microbiology
Outmoded designation: serum hepatitis, due to its historically recognized route of percutaneous transmission (interesting to note that most of the patients with "serum hepatitis" were not actually infected with HBV)
Partially double-stranded DNA virus member of the hepadnavirus family (hepatotropic DNA viruses)
Reverse-transcriptase activity associated with the viral DNA
HBSag
product of the S gene of HBV
major surface protein
several subtypes
anti-HBs is the protective antibody
extremely large production during an infection (500µg/ml or 10 trillions particles per ml)
HBcAg
core antigen
product of the C gene
HBeAg
soluble nucleocapsid protein
reliable marker of replication and infectivity
Epidemiology
Virus found in every body fluid of infected individuals (saliva, tears, CSF, seminal fluid, ascites, breast milk, gastric fluid, synovial fluid, pleural fluid, urine and even (rarely) feces)
Low infectivity with oral ingestion of the agent
Sexual and perinatal transmission are important routes
Carrier state in human (more than 200 millions in the world) is the main reservoir
Prevalence is 0.1 and 0.5% in normal population but as high as 20% in some high risk groups
Higher risk groups:
Down's syndrome
leprosy
leukemia
Hodgkin's
polyarteritis
IVDU
hemodialysis patients
spouse of acutely infected persons
sexually promiscuous people
people who required repeated transfusions (low risk with present-day blood products with screening
Clinical syndromes
Subclinical
Fulminant acute hepatitis
Chronic persistent hepatitis
Chronic active hepatitis
Hepatocellular carcinoma
Diagnosis
Serology
Comments on treatment
Acute: no therapy recommended
Chronic
recommended: interferon-alfa (2a or 2b) (4-6 months of treatment. 33% will respond)
alternative: lamivudine (duration not established)
Prevention (after transplantation for HBV-induced cirrhosis
HIV-AIDS
Microbiology
One of the four known pathogenic human retroviruses and a member of the Lentiviruses
Two recognized subtypes of HIV:
HIV-1 causes AIDS worldwide
HIV-2 produces an AIDS-like illness but appears to be less pathologic
Each virion has 2 identical copies of a single-stranded viral RNA genome
Goes through reverse transcription (RNA into double-stranded DNA)
Contains three essential genes for viral replication: gag (Group-specific AntiGen), pol (polymerase) and env (envelop)
Epidemiology
HIV is now the leading cause of death of men aged 25-40, the sixth leading cause of death of adolescent males 15-24 years of age, and the fourth leading cause of death in women 25-44 years of age.
By the year 2000, the World Health Organization estimates that there will be 40 million HIV-infected individuals worldwide.
Male homosexuality continues to be the most common mode of transmission, but I.V. drug use and heterosexual transmission continues to rise
HIV in women continues to rise
Minorities account for a disproportionate amount of AIDS
Clinical syndromes
Category A:
Asymptomatic HIV infection
Persistent generalized lymphadenopathy (PGL)
Acute (primary) HIV illness
Category B
Symptomatic, not A or C conditions
Examples include but not limited to:
Bacillary angiomatosis
Candidiasis, vulvovaginal: persistent >1 month, poorly responsive to therapy
Candidiasis, oropharyngeal
Cervical dysplasia, severe, or carcinoma in situ
Constitutional symptoms (eg, fever >38.5°C or diarrhea >1 month)
NB: attributed to HIV infection or have a clinical course or management complicated by HIV
Category C
Candidiasis: esophageal, trachea, bronchi
Coccidioidomycosis, extrapulmonary
Cryptococcosis, extrapulmonary
Cervical cancer, invasive
Cryptosporidiosis, chronic intestinal (>1 month)
CMV retinitis, or other than liver, spleen, nodes
HIV encephalopathy
Herpes simplex with mucocutaneous ulcer >1 month, bronchitis, pneumonia
Histoplasmosis: disseminated, extrapulmonary
Isosporiasis, chronic (>1 month)
Kaposi's sarcoma
Lymphoma: Burkitt's, immunoblastic, primary in brain
M. avium or M. kansasii, extrapulmonary
M. tuberculosis: pulmonary or extrapulmonary
Mycobacterium, other species disseminated or extrapulmonary
Pneumocystis carinii pneumonia
Pneumonia: recurrent (>2 episodes in 1 year)
Progressive multifocal leukoencephalopathy
Salmonella bacteremia, recurrent
Toxoplasmosis, cerebral
Wasting syndrome due to HIV
Diagnosis
Serology (ELISA and Western Blot)
PCR
CD4 counts
Comments on treatment
For more info see: AIDS
Primary:
PI (protease inhibitors) + 2 NRTIs (nucleoside reverse-transcriptase inhibitors)
Indinavir + ZDV + 3TC
Nelfinavir + d4T + ddI
(Sequinavir ± ritonavir) + [(ZDV + DDC) or (d4T + 3TC)
Alternative :
2 NRTIs (ZDV, ddI, DDC, d4T, 3TC) + NNRTI (delavirdine , nevirapine, efavirenz)
[(ZDV + 3TC) or (d4T + ddI) or (ZDV + DDC) or (d4T + 3TC)] +(efavirenz or delavirdine or nevirapine)
Paget's Disease of Bone
Definition
Condition characterised by high rates of bone resorption and disorganised immature new bone formation ® abnormal remodelling of bone
First described by Sir James Paget in 1876 and evidence of the disease found in Neanderthal man
Incidence
Affects more than 3% of population over 40 years of age around 2% of the population at age 40 to around 10% in the elderly (more than 80 years)
Relatively common in Anglo-Saxons, Britain, Germany and Australia
Britain has the highest recorded prevalence
In Australia the prevalence among British born immigrants is intermediate between the British rate and the native born Australians
Rare in Scandinavia, Russia, Italy, Asia, Africa and the Middle East
Affects American whites and blacks equally ® suggest environmental factor contributing to aetiology
Male : Female 7:6
Probably equal overall incidence but in younger individuals males slightly more frequent
Only occasionally presents in people under 50 years
There is evidence of a decline in incidence of the disease in Britain and USA
Aetiology
The primary abnormality is thought to lie in the osteoclasts but the precise cause remains unknown
Viral aetiology
suggested by the isolation of viral intra-nuclear inclusion bodies in osteoclasts on EM which resemble those of measles (Rebel 1976, Mills 1976)
Antigen to measles virus, simian virus 5 and human parainfluenza virus type 3 detected in abnormal osteoclasts (Basle 1985)
Measles virus not detected (Gordon 1991)
Canine distemper virus (CDV) in 41% of Pagetic osteoclasts, osteocytes and osteoblasts (Gordon 1991)
Slow virus type aetiology consistent with familial incidence
Ralston, 1994 investigated Pagets and normal bone with reverse-transcriptase and polymerase chain reaction
no difference in IL-1, IL-6, TNF-?, TNF-?, b-FGF, TGF-?, IGF-1
possibility that Pagets bone turnover is due to local elaboration of other osteotropic factors
Birch (Ralston) 1994 unable with PCR to detect measles and CDV aetiology for Pagets disease
Relationship to pets has been postulated but not substantiated
Genetic, as family history found in 15 - 20% of cases, and the site and extent of disease similar in family members (dominant inheritance with low penetrance (Sofaer 1983)
Extraordinary geographic variations in prevalence (see data on incidence)
Probably, Pagets disease is caused by infection with a common and widespread virus superimposed on genetic variation for susceptibility and perhaps severity of disease (Sofaer, 1983)
Interaction between hereditary and environmental factors
Geographical variations in the prevalence of Paget's disease remain unexplained and the viral hypothesis remains unproven
Also postulated
a disorder of hormonal secretion
vascular aetiology
autoimmune disease
monoclonal IgM
Clinically
Variable picture with the majority being discovered incidentally following X-Ray or elevated alkaline phosphatase
Only a minority of patients become symptomatic (5%)
Monostotic in 17% and polyostotic in 83% (pelvis 70%, Lumbar spine 50%, femur 50%, skull 45%, tibia 30%, humerus 30%, clavicle ® visible deformity in 13%, hand and foot 3 - 5%)
The disease may for many years be localised to part or the whole of one bone
Affected bones may remain asymptomatic or ® pain (dull constant ache) and become bent
Pain is worse at night, but rarely severe unless sarcoma or fracture supervene
Lesions detected on bone scan are usually painful whereas many lesions seen on X-Ray are not
Bone looks bent, feels warm (may be 5o warmer than unaffected side)and thick (osteitis deformans)
If generalised may ® headache, deafness (with impairment of hearing in 30 - 50% of cases), deformities, stiffness, limb pain and sometimes fracture and heart failure, occasionally pressure on the optic nerve may ® blindness
Facial and trigeminal nerves may also be affected
Spinal stenosis may occur ® root or cord problems infrequently or a vascular steal syndrome may ® spinal claudication
Features suggestive of pain of Pagetic origin in the back are non-specific low back pain without radiculopathy, normal or minimal findings on examination, vertebral sclerosis in radiographs, isolated vertebral involvement in bone scan and enlarged vertebra and neural arch, normal facet joints and no bony impingement
Canal stenosis occurs gradually as the expanding vertebral body reduces the canal diameter, may be kyphosis, and back ache and root pain is common
Cardiac failure associated with arterial calcification and calcification of heart valves and myocardium as well as being a high output state
About 20% of Pagets patients have fractures which may be complete or incomplete and as many as 40% ® delayed or non-union
Tinnitus and vertigo are common complaints
Coxa vara is also a feature with considerable antero-lateral bowing of the legs
When involves a joint may ® painful erosive arthritis due to altered stresses secondary to deformity and abnormal subchondral bone ® collapse or loss of resilience
X-Rays
Early ® osteoporosis circumscripta
Disease involvement usually seen at one end of the bone (generally proximal)
The bone as a whole is thick and bent
Density in the vascular stage is decreased and it is increased in the sclerotic stage
Trabeculae are coarse and widely separated
In vascular stage areas of porosis shape
Condition characterised by high rates of bone resorption and disorganised immature new bone formation ® abnormal remodelling of bone
First described by Sir James Paget in 1876 and evidence of the disease found in Neanderthal man
Incidence
Affects more than 3% of population over 40 years of age around 2% of the population at age 40 to around 10% in the elderly (more than 80 years)
Relatively common in Anglo-Saxons, Britain, Germany and Australia
Britain has the highest recorded prevalence
In Australia the prevalence among British born immigrants is intermediate between the British rate and the native born Australians
Rare in Scandinavia, Russia, Italy, Asia, Africa and the Middle East
Affects American whites and blacks equally ® suggest environmental factor contributing to aetiology
Male : Female 7:6
Probably equal overall incidence but in younger individuals males slightly more frequent
Only occasionally presents in people under 50 years
There is evidence of a decline in incidence of the disease in Britain and USA
Aetiology
The primary abnormality is thought to lie in the osteoclasts but the precise cause remains unknown
Viral aetiology
suggested by the isolation of viral intra-nuclear inclusion bodies in osteoclasts on EM which resemble those of measles (Rebel 1976, Mills 1976)
Antigen to measles virus, simian virus 5 and human parainfluenza virus type 3 detected in abnormal osteoclasts (Basle 1985)
Measles virus not detected (Gordon 1991)
Canine distemper virus (CDV) in 41% of Pagetic osteoclasts, osteocytes and osteoblasts (Gordon 1991)
Slow virus type aetiology consistent with familial incidence
Ralston, 1994 investigated Pagets and normal bone with reverse-transcriptase and polymerase chain reaction
no difference in IL-1, IL-6, TNF-?, TNF-?, b-FGF, TGF-?, IGF-1
possibility that Pagets bone turnover is due to local elaboration of other osteotropic factors
Birch (Ralston) 1994 unable with PCR to detect measles and CDV aetiology for Pagets disease
Relationship to pets has been postulated but not substantiated
Genetic, as family history found in 15 - 20% of cases, and the site and extent of disease similar in family members (dominant inheritance with low penetrance (Sofaer 1983)
Extraordinary geographic variations in prevalence (see data on incidence)
Probably, Pagets disease is caused by infection with a common and widespread virus superimposed on genetic variation for susceptibility and perhaps severity of disease (Sofaer, 1983)
Interaction between hereditary and environmental factors
Geographical variations in the prevalence of Paget's disease remain unexplained and the viral hypothesis remains unproven
Also postulated
a disorder of hormonal secretion
vascular aetiology
autoimmune disease
monoclonal IgM
Clinically
Variable picture with the majority being discovered incidentally following X-Ray or elevated alkaline phosphatase
Only a minority of patients become symptomatic (5%)
Monostotic in 17% and polyostotic in 83% (pelvis 70%, Lumbar spine 50%, femur 50%, skull 45%, tibia 30%, humerus 30%, clavicle ® visible deformity in 13%, hand and foot 3 - 5%)
The disease may for many years be localised to part or the whole of one bone
Affected bones may remain asymptomatic or ® pain (dull constant ache) and become bent
Pain is worse at night, but rarely severe unless sarcoma or fracture supervene
Lesions detected on bone scan are usually painful whereas many lesions seen on X-Ray are not
Bone looks bent, feels warm (may be 5o warmer than unaffected side)and thick (osteitis deformans)
If generalised may ® headache, deafness (with impairment of hearing in 30 - 50% of cases), deformities, stiffness, limb pain and sometimes fracture and heart failure, occasionally pressure on the optic nerve may ® blindness
Facial and trigeminal nerves may also be affected
Spinal stenosis may occur ® root or cord problems infrequently or a vascular steal syndrome may ® spinal claudication
Features suggestive of pain of Pagetic origin in the back are non-specific low back pain without radiculopathy, normal or minimal findings on examination, vertebral sclerosis in radiographs, isolated vertebral involvement in bone scan and enlarged vertebra and neural arch, normal facet joints and no bony impingement
Canal stenosis occurs gradually as the expanding vertebral body reduces the canal diameter, may be kyphosis, and back ache and root pain is common
Cardiac failure associated with arterial calcification and calcification of heart valves and myocardium as well as being a high output state
About 20% of Pagets patients have fractures which may be complete or incomplete and as many as 40% ® delayed or non-union
Tinnitus and vertigo are common complaints
Coxa vara is also a feature with considerable antero-lateral bowing of the legs
When involves a joint may ® painful erosive arthritis due to altered stresses secondary to deformity and abnormal subchondral bone ® collapse or loss of resilience
X-Rays
Early ® osteoporosis circumscripta
Disease involvement usually seen at one end of the bone (generally proximal)
The bone as a whole is thick and bent
Density in the vascular stage is decreased and it is increased in the sclerotic stage
Trabeculae are coarse and widely separated
In vascular stage areas of porosis shape
Bone Grafts
Indications
To provide stability (cortical bone best)
To provide linkage, ie replace missing bone
To stimulate osteogenesis
Bone grafts may be
Osteo-conduction
The graft provides a scaffold for bone deposition
Osteo-induction
Graft derived factors actually stimulate the recipient to invade the structure with osteogenic activity.
Physiology of remodelling and bone grafts
1. Activation
Local and systemic factors involved
2. Resorption
Appearance of osteoclasts from ? haematopoietic stem cell precursors or macrophage lineage. (pre osteoclasts may be endothelial cells, circulating monocytes, reticuloendothelial cells and fibroblasts)
3. New Bone Formation
Osteoblasts also from the marrow ® deposit osteoid ® mineralisation of the matrix.
Graft incorporation
Haematoma forms around implanted bone and only surface cells remain viable by diffusion.
Necrosis of graft follows ® inflammatory response and formation of a fibro vascular stroma.
Blood vessels and osteogenic precursors infiltrate the graft.
A neo vascular response results in increased porosity and decreased mass of the graft.
New bone formation follows and finally remodelling.
Cortical bone grafts are approximately 40-60% weaker than normal bone from 6 weeks to 6 months after transplantation. Returns to normal 1-2 years after transplant.
Factors adversely affecting incorporation
Vascularity
Infection
Foreign Material
Malnutrition
Drugs eg
(indocid, diphosphonates)
Types
Autografts
From the patient themselves, but most still dies
Vascularized autografts ® no resorption and either end of the transplanted segment heals in a way analogous to fracture healing.
Allografts
Transferred from one individual living or dead to another of the same species. Antigenicity altered by freezing / radiation. Radiation ® alters collagen ® depress graft incorporation. Osteochondral graft survival enhanced by immersion in glycerol.
Fresh grafts ® immunological response and less reliable incorporation
The sequence of events of incorporation is qualitatively similar to that for autografts, but it is delayed and less extensive (allografts are biologically inferior to autografts).
Xenografts
Bone taken from a different species, similar to allograft bone after freezing and irradiation.
Collection and distribution of donor bone in South Australia
Age limit for donation 16-60 years
Femoral Heads
Written consent required from the donor to use the bone and perform blood tests (HIV, HepB, VDRL)
Swabs taken of acetabulum and femoral head ® MCS
Biopsy of femoral head ® Histopathology
Head placed in 2 sterile bags, sterile container & un-sterile bag
Stored in -70oC ultra cold freezer
If sever osteoporosis identified bone is X-Rayed and decision made about keeping the bone
Exclusions
Hepatitis
Infection
Tumour
Rheumatoid
Alcohol / Drug abuse
Steroid treatment
Pre-senile dementia
Transfusion in last 6/12
All bone for re implantation receives 2.5 mrad of g irradiation and the bone marked ready for use.
Long bones
Consent form relatives
Tissue obtained under sterile conditions
Blood tests taken as for femoral heads
Dimensions of each bone recorded and computerised for later matching
Exclusions
Fresh bone must be 16 - 30 years old
Frozen bone can be up to 12 hours post death
Fresh bone need beating heart or in first few hours
Exclusion if in ICU > 72 hours (infection)
Allograft infection rate 10-12% and more than 80% of infected allografts are associated with clinical failure
Synthetic Grafts
Hydroxyapatite
Not biodegradable and is brittle but acts as an osteo-conductive medium
Tricalcium Phosphate
Biodegradable and is replaced by new bone but unpredictable rate of resorption and lengthy incorporation
These grafts can be used alone or mixed with autograft. Useful to fill defects where the intrinsic mechanical strength of the graft is unimportant.
Many drugs (chemotherapeutic agents, NSAIDs etc) negatively influence new bone formation in the intact skeleton and to some degree the repair associated with fractures.
Similar findings result from irradiation
Papineau Technique
Wound excision, open cancellous grafting which irradicates infection, encourages healing of the skin by granulation and results in solid bony union.
Swab for culture ® appropriate antibiotic pre-operatively
Tomograms or CT etc to define extent of sequestrum
Excision of infected tissue down to bleeding living tissue
Splint the bone if inadequate or deficient
Defect in bone must be saucerised
Development of granulation tissue ® base for subsequent graft
Secondary excision of areas not covered by granulation tissue
Within 2/52 operation for application of cancellous graft
Change dressings at 5/7 ® washing and daily dressing
Continue dressings 3/52 ( ® 3 colour changes)
By the end of the third month entire graft incorporated into granulation tissue
SSG applied if required
FWB allowed at 7/12 for osteomyelitis, 9/12 where some continuity has been preserved and 12/12 if part of the shaft was completely resected.
To provide stability (cortical bone best)
To provide linkage, ie replace missing bone
To stimulate osteogenesis
Bone grafts may be
Osteo-conduction
The graft provides a scaffold for bone deposition
Osteo-induction
Graft derived factors actually stimulate the recipient to invade the structure with osteogenic activity.
Physiology of remodelling and bone grafts
1. Activation
Local and systemic factors involved
2. Resorption
Appearance of osteoclasts from ? haematopoietic stem cell precursors or macrophage lineage. (pre osteoclasts may be endothelial cells, circulating monocytes, reticuloendothelial cells and fibroblasts)
3. New Bone Formation
Osteoblasts also from the marrow ® deposit osteoid ® mineralisation of the matrix.
Graft incorporation
Haematoma forms around implanted bone and only surface cells remain viable by diffusion.
Necrosis of graft follows ® inflammatory response and formation of a fibro vascular stroma.
Blood vessels and osteogenic precursors infiltrate the graft.
A neo vascular response results in increased porosity and decreased mass of the graft.
New bone formation follows and finally remodelling.
Cortical bone grafts are approximately 40-60% weaker than normal bone from 6 weeks to 6 months after transplantation. Returns to normal 1-2 years after transplant.
Factors adversely affecting incorporation
Vascularity
Infection
Foreign Material
Malnutrition
Drugs eg
(indocid, diphosphonates)
Types
Autografts
From the patient themselves, but most still dies
Vascularized autografts ® no resorption and either end of the transplanted segment heals in a way analogous to fracture healing.
Allografts
Transferred from one individual living or dead to another of the same species. Antigenicity altered by freezing / radiation. Radiation ® alters collagen ® depress graft incorporation. Osteochondral graft survival enhanced by immersion in glycerol.
Fresh grafts ® immunological response and less reliable incorporation
The sequence of events of incorporation is qualitatively similar to that for autografts, but it is delayed and less extensive (allografts are biologically inferior to autografts).
Xenografts
Bone taken from a different species, similar to allograft bone after freezing and irradiation.
Collection and distribution of donor bone in South Australia
Age limit for donation 16-60 years
Femoral Heads
Written consent required from the donor to use the bone and perform blood tests (HIV, HepB, VDRL)
Swabs taken of acetabulum and femoral head ® MCS
Biopsy of femoral head ® Histopathology
Head placed in 2 sterile bags, sterile container & un-sterile bag
Stored in -70oC ultra cold freezer
If sever osteoporosis identified bone is X-Rayed and decision made about keeping the bone
Exclusions
Hepatitis
Infection
Tumour
Rheumatoid
Alcohol / Drug abuse
Steroid treatment
Pre-senile dementia
Transfusion in last 6/12
All bone for re implantation receives 2.5 mrad of g irradiation and the bone marked ready for use.
Long bones
Consent form relatives
Tissue obtained under sterile conditions
Blood tests taken as for femoral heads
Dimensions of each bone recorded and computerised for later matching
Exclusions
Fresh bone must be 16 - 30 years old
Frozen bone can be up to 12 hours post death
Fresh bone need beating heart or in first few hours
Exclusion if in ICU > 72 hours (infection)
Allograft infection rate 10-12% and more than 80% of infected allografts are associated with clinical failure
Synthetic Grafts
Hydroxyapatite
Not biodegradable and is brittle but acts as an osteo-conductive medium
Tricalcium Phosphate
Biodegradable and is replaced by new bone but unpredictable rate of resorption and lengthy incorporation
These grafts can be used alone or mixed with autograft. Useful to fill defects where the intrinsic mechanical strength of the graft is unimportant.
Many drugs (chemotherapeutic agents, NSAIDs etc) negatively influence new bone formation in the intact skeleton and to some degree the repair associated with fractures.
Similar findings result from irradiation
Papineau Technique
Wound excision, open cancellous grafting which irradicates infection, encourages healing of the skin by granulation and results in solid bony union.
Swab for culture ® appropriate antibiotic pre-operatively
Tomograms or CT etc to define extent of sequestrum
Excision of infected tissue down to bleeding living tissue
Splint the bone if inadequate or deficient
Defect in bone must be saucerised
Development of granulation tissue ® base for subsequent graft
Secondary excision of areas not covered by granulation tissue
Within 2/52 operation for application of cancellous graft
Change dressings at 5/7 ® washing and daily dressing
Continue dressings 3/52 ( ® 3 colour changes)
By the end of the third month entire graft incorporated into granulation tissue
SSG applied if required
FWB allowed at 7/12 for osteomyelitis, 9/12 where some continuity has been preserved and 12/12 if part of the shaft was completely resected.
Traction
Introduction
Traction produces a reduction through the surrounding soft parts which align the fragments by their tension.
When the shaft of a long bone is fractured the elastic retraction of muscles surrounding the bone tends to produce over-riding of the fragments. This tendency is greater when the muscles are powerful and long bellied as in the thigh, when the fracture is imperfectly immobilised so that there is pain and therefore muscle spam and when the fracture is mechanically unstable because the fragments are not in apposition or because the fracture line is oblique.
Continuous traction generated by weights and pulleys in addition to causing reduction of a deformity will also produce a relative fixation of the fragments by the rigidity conferred by the surrounding soft tissue structures when under tension. It also enables maintenance of alignment while at the same time it is possible to devise apparatus which permit joint movement.
Traction may be applied through traction tapes attached to skin by adhesives or by direct pull by transfixing pins through or onto the skeleton.
Traction must always be apposed by counter traction or the pull exerted against a fixed object, otherwise it mealy pulls the patient down or off the bed.
Traction requires constant care and vigilance and is costly in terms of the length of hospital stay and all the hazards of prolonged bed rest - thromboembolism, decubiti, pneumonia and atelectasis must be considered when traction is used
Excessive traction which leads to distraction of the fracture is undesirable. Once the fracture is reduced a decreasing amount of weight is required to maintain a reduction once the muscle stretch reflex has been overcome and the fracture immobilised. For a femoral fracture no more than 10lbs should be used and for fractures of the tibia and upper limb less weight is required.
Skin Traction
Traction is applied to the skeleton through its attached soft tissued and in the adult should be used only as a temporary measure.
Skin is designed to bear compression forces and not shear. If much more than 8lbs is applied for any length of time it results in superficial layers of skin pulled off. Other difficulties such as migration of the bandage may occur with lower weights.
Skeletal Traction
First achieved by the use of tongs.
The application of traction applied by a pin transfixing bone was introduced by Fritz Steinmann. Now a threaded Denham pin is preferred to prevent early loosening of the device.
The threaded portion of the Denham pin is offset, closer to the end of the pin held in the drill chuck and should engage only the proximal cortex of the recipient long bone.
Traction by Gravity
Really only applies to fractures of the upper limb (hanging cast)
Definitions
Traction on a limb demands either a fixed point from which the traction may be exerted (fixed traction) or an equal counter-traction in the opposite direction (balanced traction)
Fixed Traction
The length of the limb remains constant and there is continuous diminution of traction force as the tone in the muscles diminishes and no further stimuli results in activation of the muscle stretch reflex.
Pull is exerted against a fixed point for example tapes are tied to the cross piece of a Thomas splint and the leg pulled down until the root of the limb abuts against the ring of the splint.
Pins in plaster is a form of fixed traction
Balanced Traction
In weight traction it is the tension in the apparatus which remains constant and the length depends on the amount of tearing of the intermuscular septum and fibrous tissue of the limb
The pull is exerted against an opposing force provided by the weight of the body when the foot of the bed is raised.
Combined Traction
May be used in conjunction with fixed traction where the weight takes up any slack in the tapes or cords while the splint maintains a reduction.
This combination facilitates less frequent checks and adjustment of the apparatus
Sliding Traction
First introduced by Pugh by applying traction tapes to the limb and fastening them to the raised foot of the bed which was then inclined head down.
He utilised this traction in the treatment of conditions such as Perthes where only one limb was fastened to the end of the bed enabling the pelvis on the opposite side to slide down the bed more thus creating traction and abduction.
The extent to which the patient slides down the bed is limited by the friction of the body against the mattress.
The traction was subsequently modified by Hendry using a mattress on a sliding frame which resulted in the same amount of traction with an inclination of 10o as that with that on a normal mattress at 30 - 40o inclination.
This is also really a form of balance traction where the amount of weight is determined by the inclination of the bed.
Specific Types of Traction
Thomas Splint Traction
Hugh Owen Thomas introduced his splint which he called "The Knee Appliance" in 1875.
The method of Hugh Owen Thomas uses fixed traction with the counter traction being applied against the perineum by the ring of the splint. This is in contrast to other methods using weight traction which is countered by the weight of the body.
Backward angulation of the distal fragment can never be corrected by traction in the axis of the femur which only results in elongation with persistence of the deformity.
Traction produces a reduction through the surrounding soft parts which align the fragments by their tension.
When the shaft of a long bone is fractured the elastic retraction of muscles surrounding the bone tends to produce over-riding of the fragments. This tendency is greater when the muscles are powerful and long bellied as in the thigh, when the fracture is imperfectly immobilised so that there is pain and therefore muscle spam and when the fracture is mechanically unstable because the fragments are not in apposition or because the fracture line is oblique.
Continuous traction generated by weights and pulleys in addition to causing reduction of a deformity will also produce a relative fixation of the fragments by the rigidity conferred by the surrounding soft tissue structures when under tension. It also enables maintenance of alignment while at the same time it is possible to devise apparatus which permit joint movement.
Traction may be applied through traction tapes attached to skin by adhesives or by direct pull by transfixing pins through or onto the skeleton.
Traction must always be apposed by counter traction or the pull exerted against a fixed object, otherwise it mealy pulls the patient down or off the bed.
Traction requires constant care and vigilance and is costly in terms of the length of hospital stay and all the hazards of prolonged bed rest - thromboembolism, decubiti, pneumonia and atelectasis must be considered when traction is used
Excessive traction which leads to distraction of the fracture is undesirable. Once the fracture is reduced a decreasing amount of weight is required to maintain a reduction once the muscle stretch reflex has been overcome and the fracture immobilised. For a femoral fracture no more than 10lbs should be used and for fractures of the tibia and upper limb less weight is required.
Skin Traction
Traction is applied to the skeleton through its attached soft tissued and in the adult should be used only as a temporary measure.
Skin is designed to bear compression forces and not shear. If much more than 8lbs is applied for any length of time it results in superficial layers of skin pulled off. Other difficulties such as migration of the bandage may occur with lower weights.
Skeletal Traction
First achieved by the use of tongs.
The application of traction applied by a pin transfixing bone was introduced by Fritz Steinmann. Now a threaded Denham pin is preferred to prevent early loosening of the device.
The threaded portion of the Denham pin is offset, closer to the end of the pin held in the drill chuck and should engage only the proximal cortex of the recipient long bone.
Traction by Gravity
Really only applies to fractures of the upper limb (hanging cast)
Definitions
Traction on a limb demands either a fixed point from which the traction may be exerted (fixed traction) or an equal counter-traction in the opposite direction (balanced traction)
Fixed Traction
The length of the limb remains constant and there is continuous diminution of traction force as the tone in the muscles diminishes and no further stimuli results in activation of the muscle stretch reflex.
Pull is exerted against a fixed point for example tapes are tied to the cross piece of a Thomas splint and the leg pulled down until the root of the limb abuts against the ring of the splint.
Pins in plaster is a form of fixed traction
Balanced Traction
In weight traction it is the tension in the apparatus which remains constant and the length depends on the amount of tearing of the intermuscular septum and fibrous tissue of the limb
The pull is exerted against an opposing force provided by the weight of the body when the foot of the bed is raised.
Combined Traction
May be used in conjunction with fixed traction where the weight takes up any slack in the tapes or cords while the splint maintains a reduction.
This combination facilitates less frequent checks and adjustment of the apparatus
Sliding Traction
First introduced by Pugh by applying traction tapes to the limb and fastening them to the raised foot of the bed which was then inclined head down.
He utilised this traction in the treatment of conditions such as Perthes where only one limb was fastened to the end of the bed enabling the pelvis on the opposite side to slide down the bed more thus creating traction and abduction.
The extent to which the patient slides down the bed is limited by the friction of the body against the mattress.
The traction was subsequently modified by Hendry using a mattress on a sliding frame which resulted in the same amount of traction with an inclination of 10o as that with that on a normal mattress at 30 - 40o inclination.
This is also really a form of balance traction where the amount of weight is determined by the inclination of the bed.
Specific Types of Traction
Thomas Splint Traction
Hugh Owen Thomas introduced his splint which he called "The Knee Appliance" in 1875.
The method of Hugh Owen Thomas uses fixed traction with the counter traction being applied against the perineum by the ring of the splint. This is in contrast to other methods using weight traction which is countered by the weight of the body.
Backward angulation of the distal fragment can never be corrected by traction in the axis of the femur which only results in elongation with persistence of the deformity.
Tibia Fractures
Proximal Tibial Fractures
Mechanism
young pt - high energy trauma
old pt minor fall
Classification AO
extrarticular
intraarticular, unicondylar
intraarticular, bicondylar
60% are lat plateau
15% are med plateau
25% involve both
Evaluation
assess assoc injuries, neurovasc examination
XRay: plain films, biplanar tomography, CT
Treatment
Extraarticular
CR if necessary, AKPOP or cast brace
Intraarticular
Undisplaced
AKPOP/ cast brace
Displaced
ORIF / BG/ cast brace for split depression
simple depression fracture may be amenable to elevation without plating using an arthroscopic assisted technique
type C fracture- often very comminuted, difficult to reconstruc, thus CR/cast bracing often preferable
Note association with meniscal lesions in ~20%
collateral or cruciate lig injuries in ~20%
Complications
nonunion
rare
malunion
more common with nonop treatment
Bicondylar fracture
knee instability due to either malunion or ligament injury
infection
more common in bicondylar fracture - increased op time, exposure, hardware
Prognosis
ref: Anglen and Healy "tibial plateau fractures" Orthopaedics 11:1527-1534, 1988
Undisplaced fracture 85% satisfactory with nonop treatment
Displaced fracture 78% satisfactory with ORIF, 54% with nonop treatment
Lachiewicz and Funcik "factors influencing the results of ORIF of tibial plateau fractures"
CORR 259: 210-215, 1990
44 fractures, 2.7 yr FU, 91% good or excellent, implant removal needed in 1/3 pts
Tibial Spine Fractures
Mechanism
hyper extension or hyperflexion® avulsion
Classification
Meyers and McKeever "Fractures of the intercondylar eminence of the tibia"
JBJS 52A: 1677-1684, 1970
Type 1: undisplaced
Type 2: displaced hinging posteriorly
Type 3: displaced with complete separation
Treatment
Type 1 + 2 CR with knee in extension likely to be successful- if not ORIF
Type 3 ORIF
Prognosis
good , low incidence of late instability
if malunion may get impingement in extension
Avulsion of the Tibial Tubercle
ref: Ogden etal "fractures of the tibial tuberosity in adolescents" JBJS 62A:205-215, 1980
Mechanism
usually in vigorous sports- violent contraction of quads in sudden acceleration or deceleration
Classification
Type 1 fracture
across the secondary ossification centre level with the post border of the inserting patellar tendon
Type 2 fracture
at the junction of the primary and secondary ossification centres
of the prox tibial epiphysis
Type 3
fracture propagates across the primary ossification centre= SH type 3
Treatment
ORIF , protect in extension , ROM exs
Prognosis
excellent
Tibial Shaft Fractures
Classification AO
Type A simple
a single circumferential disruption of the diaphysis - may be:
Spiral
Oblique ( angle more than 30 deg)
Transverse (angle less than 30 deg)
Type B multifragmentary: wedge
a fracture with one or more intermediate fragments in which after reduction, there is some contact bw the main fragments- may be:
Spiral wedge
Bending wedge
Fragmented wedge
Type C Multifragmentary: complex
a fracture with one or more intermediate fragments in which after reduction , there is no contact bw the main prox and distal fragments- may be:
Spiral
Segmental
Irregular
Treatment - closed injury
Nonoperative
best for fracture without significant comminution, shortening or displacement at the time of fracture. ie low energy fracture
AKPOP for 6/52, then convert to cast brace or PTB
union in approx 16 wks for simple fracture, longer for more complex injury (av 18 wks)
ref: Sarmiento etal "Tibial shaft fractures treated with functional braces: experience with 780 fractures" JBJS 71B: 602-609, 1989
90% healed with 1cm or less shortening
nonunion rate 2.5%
Operative
indicated in:
pt requires early return to work
displaced ie higher energy fracture
Failure of closed treatment
IM nailing:
ref: Hooper etal "Conservative management or closed nailing for tibial shaft fractures : a randomised prospective trial " JBJS 73B: 83-85, 1991
infection rate ~ 1-2%
angulatory deformities rare
shorter hospital stay, less OPD visits
earlier return to work
Treatment - Open Fractures
Wound management as for any compound fracture
IM Nailing
Court-Brown etal "Infection after intramedullary nailing of the tibia" JBJS 74B: 770-774, 1992
Tornetta etal " treatment of grade 3B open tibial fractures- a prospective randomised comparison of external fixation and nonreamed nailing" JBJS 76A:13-19, 1994
Grade 1
IM nailing - same figures as for closed fracture
Grade 2
infection 3.8%
Grade 3
A: infection 5.6%
B: infection 12.5%
External fixation:
Use for grade 3B and 3C
rates of infection same as nailing for grade 3B with added problem of pin tract infection, delayed union also a feature of ex fixation.
sometimes need to convert from ex fix to IM nail- risk of infection in the face of recent pin tract infection is ~ 20%, However if the ex fix is removed within 3 wks of application + wait another 2 wks,can nail with infection rate of ~ 5%
Ref: Johansen etal " Objective criteria accurately predict amputation following lower extremity trauma " J Trauma 30: 568-573, 1990
The MESS
1. Skeletal/ soft tissue injury
a. Low energy
eg simple fracture, civilian gunshot
1
b. Medium energy
eg open or multiple fractures, dislocation
2
c. High energy
eg close range shotgun, military gunshot, crush
3
d.
Mechanism
young pt - high energy trauma
old pt minor fall
Classification AO
extrarticular
intraarticular, unicondylar
intraarticular, bicondylar
60% are lat plateau
15% are med plateau
25% involve both
Evaluation
assess assoc injuries, neurovasc examination
XRay: plain films, biplanar tomography, CT
Treatment
Extraarticular
CR if necessary, AKPOP or cast brace
Intraarticular
Undisplaced
AKPOP/ cast brace
Displaced
ORIF / BG/ cast brace for split depression
simple depression fracture may be amenable to elevation without plating using an arthroscopic assisted technique
type C fracture- often very comminuted, difficult to reconstruc, thus CR/cast bracing often preferable
Note association with meniscal lesions in ~20%
collateral or cruciate lig injuries in ~20%
Complications
nonunion
rare
malunion
more common with nonop treatment
Bicondylar fracture
knee instability due to either malunion or ligament injury
infection
more common in bicondylar fracture - increased op time, exposure, hardware
Prognosis
ref: Anglen and Healy "tibial plateau fractures" Orthopaedics 11:1527-1534, 1988
Undisplaced fracture 85% satisfactory with nonop treatment
Displaced fracture 78% satisfactory with ORIF, 54% with nonop treatment
Lachiewicz and Funcik "factors influencing the results of ORIF of tibial plateau fractures"
CORR 259: 210-215, 1990
44 fractures, 2.7 yr FU, 91% good or excellent, implant removal needed in 1/3 pts
Tibial Spine Fractures
Mechanism
hyper extension or hyperflexion® avulsion
Classification
Meyers and McKeever "Fractures of the intercondylar eminence of the tibia"
JBJS 52A: 1677-1684, 1970
Type 1: undisplaced
Type 2: displaced hinging posteriorly
Type 3: displaced with complete separation
Treatment
Type 1 + 2 CR with knee in extension likely to be successful- if not ORIF
Type 3 ORIF
Prognosis
good , low incidence of late instability
if malunion may get impingement in extension
Avulsion of the Tibial Tubercle
ref: Ogden etal "fractures of the tibial tuberosity in adolescents" JBJS 62A:205-215, 1980
Mechanism
usually in vigorous sports- violent contraction of quads in sudden acceleration or deceleration
Classification
Type 1 fracture
across the secondary ossification centre level with the post border of the inserting patellar tendon
Type 2 fracture
at the junction of the primary and secondary ossification centres
of the prox tibial epiphysis
Type 3
fracture propagates across the primary ossification centre= SH type 3
Treatment
ORIF , protect in extension , ROM exs
Prognosis
excellent
Tibial Shaft Fractures
Classification AO
Type A simple
a single circumferential disruption of the diaphysis - may be:
Spiral
Oblique ( angle more than 30 deg)
Transverse (angle less than 30 deg)
Type B multifragmentary: wedge
a fracture with one or more intermediate fragments in which after reduction, there is some contact bw the main fragments- may be:
Spiral wedge
Bending wedge
Fragmented wedge
Type C Multifragmentary: complex
a fracture with one or more intermediate fragments in which after reduction , there is no contact bw the main prox and distal fragments- may be:
Spiral
Segmental
Irregular
Treatment - closed injury
Nonoperative
best for fracture without significant comminution, shortening or displacement at the time of fracture. ie low energy fracture
AKPOP for 6/52, then convert to cast brace or PTB
union in approx 16 wks for simple fracture, longer for more complex injury (av 18 wks)
ref: Sarmiento etal "Tibial shaft fractures treated with functional braces: experience with 780 fractures" JBJS 71B: 602-609, 1989
90% healed with 1cm or less shortening
nonunion rate 2.5%
Operative
indicated in:
pt requires early return to work
displaced ie higher energy fracture
Failure of closed treatment
IM nailing:
ref: Hooper etal "Conservative management or closed nailing for tibial shaft fractures : a randomised prospective trial " JBJS 73B: 83-85, 1991
infection rate ~ 1-2%
angulatory deformities rare
shorter hospital stay, less OPD visits
earlier return to work
Treatment - Open Fractures
Wound management as for any compound fracture
IM Nailing
Court-Brown etal "Infection after intramedullary nailing of the tibia" JBJS 74B: 770-774, 1992
Tornetta etal " treatment of grade 3B open tibial fractures- a prospective randomised comparison of external fixation and nonreamed nailing" JBJS 76A:13-19, 1994
Grade 1
IM nailing - same figures as for closed fracture
Grade 2
infection 3.8%
Grade 3
A: infection 5.6%
B: infection 12.5%
External fixation:
Use for grade 3B and 3C
rates of infection same as nailing for grade 3B with added problem of pin tract infection, delayed union also a feature of ex fixation.
sometimes need to convert from ex fix to IM nail- risk of infection in the face of recent pin tract infection is ~ 20%, However if the ex fix is removed within 3 wks of application + wait another 2 wks,can nail with infection rate of ~ 5%
Ref: Johansen etal " Objective criteria accurately predict amputation following lower extremity trauma " J Trauma 30: 568-573, 1990
The MESS
1. Skeletal/ soft tissue injury
a. Low energy
eg simple fracture, civilian gunshot
1
b. Medium energy
eg open or multiple fractures, dislocation
2
c. High energy
eg close range shotgun, military gunshot, crush
3
d.
Spine Fractures
Cervical Spine Fractures
Anatomy
spinal cord occupies ~ 35% of canal at the level of the Atlas and ~ 50% of the canal in the lower cervical region (C2-7) and the thoracolumbar spine
History
nature of incident
any neurological symptoms, any change in neurol status
LOC
head/ pectoral girdle injury
Examination
observe
head control
head injuries, pectoral girdle injuries: contusion
voluntary movement of all 4 limbs
Priapism
any limitation of movement of the pts head to either side
Palpate
tenderness over head + back off neck
step in spines
local haematoma
Neurological exam
Sensory
C2
back of head
C3
front of neck
C4
lat and inf over clavicles down to 2nd interspace
C5 - T1
upper limb
T2
below nipple
T10
unbilicus
L1
groin
L2- S2
lower limb
S3- S5 + coccygeal roots
perianal/ saddle
-once the sensory level is determined, examine distally for any evidence of sparing.
Sacral sparing indicates preservation of the lateral columns and recovery of lost muscle function is quite likely
Motor
after the sensory exam the diagnosis of a root lesion or cord lesion can be made and the completeness determined
Examine sequential nerve roots
C4
pt breaths diapragmatically
C5/6
biceps
C5
deltoid
C6
ECRL/ECRB
C7/8
triceps
C7
EDC
C8
FDP/FDP
T1
intrinsics
L1/2
adductors
L3/4
knee extension
L5/1
knee flexion
L4
tib ant
L5
EHL/ peronei
S1/2
ankle plantar flexion
Rectal inability of the pt to feel the finger in the rectum confirms a complete sensory lesion
If sphincter doesn't contract voluntarily about the finger + there are no other signs of voluntary motor power,complete motor paralysis is confirmed
Bulbocavernosus reflex: a squeeze on the glans, a tap on the mons or a tug on the catheter stimulating the trigone of the bladder causes reflex contraction of the anal sphincter about the gloved finger
If spinal shock is present a complete lesion cannot be diagnosed with certainty- if the bulbocavernosus has not returned in 24 hrs its absence is due to complete lesion as spinal shock resolves within 24 hrs
Spinal Cord Lesions
Spinal Shock
Wrt spinal cord injury = a spinal cord nervous tissue dysfunction based on physiologic dysfunction rather than structural disruption.
Spinal shock has resolved when the reflex arcs below the level of the injury begin to function again
Root injuries
are essentially peripheral nerve injuries , partial recovery is expected
root avulsion is rare except in plexus injury
Incomplete spinal cord lesions
any sparing distal to the injury = incomplete lesion= possible recovery
the greater the sparing the greater the prognosis
Brown- Sequard
an injury to either side of the cord (hemisection)
ipsilateral: muscle paralysis and jt position/ vibration loss
contralateral: pain and temperature loss
- good prognosis, 90% regain bladder / bowel function + walk
Central cord syndrome
most common incomplete cord injury, assoc with extension injury to Cx spine in middle aged pt
Impact direct to the central grey matter®severe flaccid LMN paralysis of the upper limbs
Damage to the central portion of the corticospinal and spinothalamic long tracts in the white matter®UMN spastic paralysis of the lower limbs and trunk
The sacral tracts are peripheral and are usually spared and the pt has sacral sparing
Prognosis
50-60% have progressive return of motor and sensory function to lower limbs- but poor recovery of hand function due to irreversible damage to the central grey matter
Anterior cord syndrome
complete motor and sensory loss apart from dorsal column sparing with deep pressure/ proprioception/ vibration as only remaining modality
prognosis
good if recovery progressive within 24 hrs
after 24 hrs prognosis poor
10-15% have recovery
Posterior cord syndrome
loss of deep pressure/ proprioception/ vibration only
Complete Cord Injuries
Frankel classification of Neurological Deficits in pts with Cord injuries
ref: Frankel etal "The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia: Part 1."
Paraplegia 7: 179-192, 1969
Types
absent motor and sensory function
sensation present, motor function absent
sensation present, motor function present but not useful (gd 2-3/5)
sensation present motor function active and useful ( gd 4-5/5)
normal motor and sensory function
Assessment of Cx cord injuries
Plain XR
direct XR evidence of instability
Increased angulation bw spinous processes more than 11 deg than in adjacent segments
Ant or post translation of the vertebral bodies more than 3.5 mm
segmental disc space widening on lat XR
facet jt widening
malalignment of spinous processes of ant view
Rotation of the facets on lat XR
at tilt of vertebral body on ant XR
XR findings suggestive of unstable injuries
Increased retro pharyngeal space - ant to C3 normal not more than 3 mm
C4 + below- normal varies 8-10 mm
minimal compression fracture of ant vertebral bodies
Avulsion fracture at or near insertion of spinal ligs
nondisplaced fracture lines
Tomography
good for posterior elements, dens fracture
CT
assess bony encroachment on canal , best method for accurate bone definition
MRI
evaluate neural elements
disc disruption
ligamentous disruption
Stress XR's
flexion/ extension contraindicated in altered state of consciousness
Anatomy
spinal cord occupies ~ 35% of canal at the level of the Atlas and ~ 50% of the canal in the lower cervical region (C2-7) and the thoracolumbar spine
History
nature of incident
any neurological symptoms, any change in neurol status
LOC
head/ pectoral girdle injury
Examination
observe
head control
head injuries, pectoral girdle injuries: contusion
voluntary movement of all 4 limbs
Priapism
any limitation of movement of the pts head to either side
Palpate
tenderness over head + back off neck
step in spines
local haematoma
Neurological exam
Sensory
C2
back of head
C3
front of neck
C4
lat and inf over clavicles down to 2nd interspace
C5 - T1
upper limb
T2
below nipple
T10
unbilicus
L1
groin
L2- S2
lower limb
S3- S5 + coccygeal roots
perianal/ saddle
-once the sensory level is determined, examine distally for any evidence of sparing.
Sacral sparing indicates preservation of the lateral columns and recovery of lost muscle function is quite likely
Motor
after the sensory exam the diagnosis of a root lesion or cord lesion can be made and the completeness determined
Examine sequential nerve roots
C4
pt breaths diapragmatically
C5/6
biceps
C5
deltoid
C6
ECRL/ECRB
C7/8
triceps
C7
EDC
C8
FDP/FDP
T1
intrinsics
L1/2
adductors
L3/4
knee extension
L5/1
knee flexion
L4
tib ant
L5
EHL/ peronei
S1/2
ankle plantar flexion
Rectal inability of the pt to feel the finger in the rectum confirms a complete sensory lesion
If sphincter doesn't contract voluntarily about the finger + there are no other signs of voluntary motor power,complete motor paralysis is confirmed
Bulbocavernosus reflex: a squeeze on the glans, a tap on the mons or a tug on the catheter stimulating the trigone of the bladder causes reflex contraction of the anal sphincter about the gloved finger
If spinal shock is present a complete lesion cannot be diagnosed with certainty- if the bulbocavernosus has not returned in 24 hrs its absence is due to complete lesion as spinal shock resolves within 24 hrs
Spinal Cord Lesions
Spinal Shock
Wrt spinal cord injury = a spinal cord nervous tissue dysfunction based on physiologic dysfunction rather than structural disruption.
Spinal shock has resolved when the reflex arcs below the level of the injury begin to function again
Root injuries
are essentially peripheral nerve injuries , partial recovery is expected
root avulsion is rare except in plexus injury
Incomplete spinal cord lesions
any sparing distal to the injury = incomplete lesion= possible recovery
the greater the sparing the greater the prognosis
Brown- Sequard
an injury to either side of the cord (hemisection)
ipsilateral: muscle paralysis and jt position/ vibration loss
contralateral: pain and temperature loss
- good prognosis, 90% regain bladder / bowel function + walk
Central cord syndrome
most common incomplete cord injury, assoc with extension injury to Cx spine in middle aged pt
Impact direct to the central grey matter®severe flaccid LMN paralysis of the upper limbs
Damage to the central portion of the corticospinal and spinothalamic long tracts in the white matter®UMN spastic paralysis of the lower limbs and trunk
The sacral tracts are peripheral and are usually spared and the pt has sacral sparing
Prognosis
50-60% have progressive return of motor and sensory function to lower limbs- but poor recovery of hand function due to irreversible damage to the central grey matter
Anterior cord syndrome
complete motor and sensory loss apart from dorsal column sparing with deep pressure/ proprioception/ vibration as only remaining modality
prognosis
good if recovery progressive within 24 hrs
after 24 hrs prognosis poor
10-15% have recovery
Posterior cord syndrome
loss of deep pressure/ proprioception/ vibration only
Complete Cord Injuries
Frankel classification of Neurological Deficits in pts with Cord injuries
ref: Frankel etal "The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia: Part 1."
Paraplegia 7: 179-192, 1969
Types
absent motor and sensory function
sensation present, motor function absent
sensation present, motor function present but not useful (gd 2-3/5)
sensation present motor function active and useful ( gd 4-5/5)
normal motor and sensory function
Assessment of Cx cord injuries
Plain XR
direct XR evidence of instability
Increased angulation bw spinous processes more than 11 deg than in adjacent segments
Ant or post translation of the vertebral bodies more than 3.5 mm
segmental disc space widening on lat XR
facet jt widening
malalignment of spinous processes of ant view
Rotation of the facets on lat XR
at tilt of vertebral body on ant XR
XR findings suggestive of unstable injuries
Increased retro pharyngeal space - ant to C3 normal not more than 3 mm
C4 + below- normal varies 8-10 mm
minimal compression fracture of ant vertebral bodies
Avulsion fracture at or near insertion of spinal ligs
nondisplaced fracture lines
Tomography
good for posterior elements, dens fracture
CT
assess bony encroachment on canal , best method for accurate bone definition
MRI
evaluate neural elements
disc disruption
ligamentous disruption
Stress XR's
flexion/ extension contraindicated in altered state of consciousness
Scapular and Clavicle Fractures
Sternoclavicular Joint
Anatomy
Diarthrodial jt, both jt surfaces covered by fibrocartilage
Artic surface of clavicle larger than that of the sternum, jt surfaces not congruent
Ligaments
intraarticular disc- fibrocartilage, divides jt into 2 cavities, rarely perforated
- runs from synchondral junction of 1st rib + sternum to sup + post aspect of med clavicle. Ant and post it blends with the capsule.
- acts to prevent med displacement of the med clavicle
Costoclavicular lig ( = rhomboid lig) - form the upper surface of the 1st rib and synchondral junction with the sternum to the rhomboid tubercle on the inf surface of the clavicle. Has 2 laminae - run in same pattern as the int and ext oblique muscles.
- ant fibres act to prevent upward motion of the clavicle
- post fibres act to prevent downward motion of the clavicle
Interclavicular lig - connects the superomed ends of each clavicle with the capsule and the upper sternum
- acts to prevent upward motion of the med clavicle
Capsule - thickened ant and post with the post being strongest
- prevents upward displacement of the med clavicle
Ossification
the clavicle is the 1st long bone of the body to ossify ( 5th intrauterine wk)
the med epiphysis is the last to appear (~ 18 ) and last to close ( ~ 25)
The capsule attaches to the epiphysis and the costoclavicular lig attaches to the metaphysis.
Thus in a SH 1 injury the costoclavicular lig is detached from the metaphysis or torn while the capsule and epiphysis remain intact.
In a SH 2 injury the costoclavicular lig remains attached to the distal fragment comprising the epiphysis and a piece of metaphysis
Classification
Anterior - most common, caused by lat compression with the shoulder rolling backward
Posterior - uncommon, caused by lat compression with the shoulder rolling forward
Injuries to the jt can be
sprain
acute dislocation
recurrent dislocation
unreduced dislocation
Symptoms and signs
severe pain increased by any movement of the arm ( post more painful than ant )
the affected shoulder appears shortened and thrust forward cf the normal side
Anterior
the med clavicle can be observed and palpated ant to the sternum
med clavicle may be fixed or mobile
Posterior
the med prominence of the normal clavicle is absent
the med clavicle is not palpable
may be venous congestion
breathing or swallowing difficulties
pneumothorax
shock due to damage to great vessels
XRay
AP view difficult to interpret
Hobbs view - pt seated, leans over table with arms up and head resting in hands, cassette on table ~ under pts neck, XR beam directed vertically down
Serendipity view : pt supine, 40 deg cephalic tilt view
Tomography
CT - gold standard
Treatment
Sprain: Rest, sling, gradual return to activity
Dislocation, anterior
most ant dislocations are unstable - notwithstanding -
CR - GA, pt supine, sandbag under centre of back
assistant pushes shoulders back
surgeon pushes clavicle back into place
in most cases this will not remain reduced - pt counselled that the risks of ORIF outweigh the cosmetic benefits of reduction
postreduction - if stable - clavicular rings to maintain position
if unstable - sling, gradual return to activity
NB cosmetic and functional deficit minimal if unreduced
Dislocation, posterior
once reduced are usually stable
may need to involve thoracic surgeon if mediastinal structures compromised
CR - GA, pt supine, sandbag under centre of back
gentle traction in line of clavicle, countertraction by assistant - this alone may reduce the dislocation
if not reduced, add manipulation with a towel clip - will reduce with clunk
rarely CR fails therefore ® OR
same position, free drape arm
involve thoracic surgeon
incision parallel to med 7-10 cm clavicle
reduction -
if stable treat as for CR
if unstable - excise the med 1- 1.5 cm clavicle and secure the remaining clavicle to the 1st rib with dacron tape
post op - clavicular rings 6 wks
Unreduced dislocation
Anterior
functional and cosmetic deficit minimal if any - no treatment indicated
Posterior
due to risk to mediastinal structures - OR indicated ( as above)
Clavicular Fractures
Classification
Type 1
middle 1/3 fractures ~ 80%
Type 2
distal 1/3 fractures ~ 15%
minimal displacement bw conoid and trapezoid ligs
ie both ligs intact
(a). fracture med to coracoclavicular ligs - displaced
(b). fracture bw conoid and trapezoid lig - displaced - ie conoid lig ruptured, trapezoid lig intact
intraartic fracture of AC jt - no lig disruption or displacement
Paediatric: ligaments intact attached to periosteum while prox frag displaces up through the disrupted periosteal sleeve
Comminuted with ligaments not attached prox or dist, but an inferior, comminuted fragment
Type 3 prox 1/3 fractures ~ 5%
minimal displacement
signif displacement ie ligs ruptured
intraarticular
epiphyseal separation - children and young adults
comminuted
Assoc injuries
Skeletal AC and SC dislocations
head and neck injuries
fracture 1st rib
Scapulothoracic dissociation
Lung and pleura PTX or haemothorax
tears of trachea or main bronchi
Brachial Plexus ulnar n most often involved in direct trauma
Vascular unusual - vessels protected by subclavius and deep cervical fascia
Mechanisms of injury
birth trauma clavicle compressed against maternal symphysis in a cephalic presentation or direct traction in a breech deli
Anatomy
Diarthrodial jt, both jt surfaces covered by fibrocartilage
Artic surface of clavicle larger than that of the sternum, jt surfaces not congruent
Ligaments
intraarticular disc- fibrocartilage, divides jt into 2 cavities, rarely perforated
- runs from synchondral junction of 1st rib + sternum to sup + post aspect of med clavicle. Ant and post it blends with the capsule.
- acts to prevent med displacement of the med clavicle
Costoclavicular lig ( = rhomboid lig) - form the upper surface of the 1st rib and synchondral junction with the sternum to the rhomboid tubercle on the inf surface of the clavicle. Has 2 laminae - run in same pattern as the int and ext oblique muscles.
- ant fibres act to prevent upward motion of the clavicle
- post fibres act to prevent downward motion of the clavicle
Interclavicular lig - connects the superomed ends of each clavicle with the capsule and the upper sternum
- acts to prevent upward motion of the med clavicle
Capsule - thickened ant and post with the post being strongest
- prevents upward displacement of the med clavicle
Ossification
the clavicle is the 1st long bone of the body to ossify ( 5th intrauterine wk)
the med epiphysis is the last to appear (~ 18 ) and last to close ( ~ 25)
The capsule attaches to the epiphysis and the costoclavicular lig attaches to the metaphysis.
Thus in a SH 1 injury the costoclavicular lig is detached from the metaphysis or torn while the capsule and epiphysis remain intact.
In a SH 2 injury the costoclavicular lig remains attached to the distal fragment comprising the epiphysis and a piece of metaphysis
Classification
Anterior - most common, caused by lat compression with the shoulder rolling backward
Posterior - uncommon, caused by lat compression with the shoulder rolling forward
Injuries to the jt can be
sprain
acute dislocation
recurrent dislocation
unreduced dislocation
Symptoms and signs
severe pain increased by any movement of the arm ( post more painful than ant )
the affected shoulder appears shortened and thrust forward cf the normal side
Anterior
the med clavicle can be observed and palpated ant to the sternum
med clavicle may be fixed or mobile
Posterior
the med prominence of the normal clavicle is absent
the med clavicle is not palpable
may be venous congestion
breathing or swallowing difficulties
pneumothorax
shock due to damage to great vessels
XRay
AP view difficult to interpret
Hobbs view - pt seated, leans over table with arms up and head resting in hands, cassette on table ~ under pts neck, XR beam directed vertically down
Serendipity view : pt supine, 40 deg cephalic tilt view
Tomography
CT - gold standard
Treatment
Sprain: Rest, sling, gradual return to activity
Dislocation, anterior
most ant dislocations are unstable - notwithstanding -
CR - GA, pt supine, sandbag under centre of back
assistant pushes shoulders back
surgeon pushes clavicle back into place
in most cases this will not remain reduced - pt counselled that the risks of ORIF outweigh the cosmetic benefits of reduction
postreduction - if stable - clavicular rings to maintain position
if unstable - sling, gradual return to activity
NB cosmetic and functional deficit minimal if unreduced
Dislocation, posterior
once reduced are usually stable
may need to involve thoracic surgeon if mediastinal structures compromised
CR - GA, pt supine, sandbag under centre of back
gentle traction in line of clavicle, countertraction by assistant - this alone may reduce the dislocation
if not reduced, add manipulation with a towel clip - will reduce with clunk
rarely CR fails therefore ® OR
same position, free drape arm
involve thoracic surgeon
incision parallel to med 7-10 cm clavicle
reduction -
if stable treat as for CR
if unstable - excise the med 1- 1.5 cm clavicle and secure the remaining clavicle to the 1st rib with dacron tape
post op - clavicular rings 6 wks
Unreduced dislocation
Anterior
functional and cosmetic deficit minimal if any - no treatment indicated
Posterior
due to risk to mediastinal structures - OR indicated ( as above)
Clavicular Fractures
Classification
Type 1
middle 1/3 fractures ~ 80%
Type 2
distal 1/3 fractures ~ 15%
minimal displacement bw conoid and trapezoid ligs
ie both ligs intact
(a). fracture med to coracoclavicular ligs - displaced
(b). fracture bw conoid and trapezoid lig - displaced - ie conoid lig ruptured, trapezoid lig intact
intraartic fracture of AC jt - no lig disruption or displacement
Paediatric: ligaments intact attached to periosteum while prox frag displaces up through the disrupted periosteal sleeve
Comminuted with ligaments not attached prox or dist, but an inferior, comminuted fragment
Type 3 prox 1/3 fractures ~ 5%
minimal displacement
signif displacement ie ligs ruptured
intraarticular
epiphyseal separation - children and young adults
comminuted
Assoc injuries
Skeletal AC and SC dislocations
head and neck injuries
fracture 1st rib
Scapulothoracic dissociation
Lung and pleura PTX or haemothorax
tears of trachea or main bronchi
Brachial Plexus ulnar n most often involved in direct trauma
Vascular unusual - vessels protected by subclavius and deep cervical fascia
Mechanisms of injury
birth trauma clavicle compressed against maternal symphysis in a cephalic presentation or direct traction in a breech deli
Pelvic and Acetabular Fractures
General
Classification (Tile)
Type A: Stable
A1
Fracture not involving the ring
avulsion fracture of ASIS,AIIS or ischium
fracture of iliac wing
A2
Stable minimally displaced ring fractures
Type B:
Rotationally unstable / Vertically stable
B1
Open book
B2
Lateral compression (ipsilateral post and ant fractures)
Stage
separation of the symphysis less than 2.5 cm
-implies no post lesion
separation of symphysis more than 2.5 cm, unilat
more than 2.5 cm, bilat
-implies disruption of sacrospinous + ant sacroiliac ligs
B3
Lateral compression (contra-lateral post and ant fractures= bucket handle)
- the rotation of the bucket handle can cause gross pelvic deformity or significant LLD
External fixation ® definitive treatment, to aid or maintain reduction
Type C:
Rotationally and vertically unstable
C1: Unilateral
C2: Bilateral
C3: Associated with acetabular fractures
External fixation ® partial stability ® reduce bleeding, relieve pain and aid in nursing the patient
Posterior stabilisation may also be required
ref : Tile " pelvic ring fractures :should they be fixed" JBJS 70B:1-12, 1988
Classification (Apley)
1. Avulsions:
Due to violent muscle action
Sartorius from ASIS
Rectus femoris from AIIS
Adductor longus from pubis
Hamstrings form ischial tuberosity
Treatment ® rest and reassurance
2. Ring fractures:
Stable fractures ® symptomatic treatment
Disruption of posterior structures ® 4 - 6 weeks RIB
Unstable fractures;
Four poster
Open book
Malgaine type
Direct fractures of the iliac wing ® bed rest
Stress fractures of the pubis / pubic rami are not uncommon in osteoporotic patients
3. Acetabular fractures:
Anterior pillar (not WB part of joint)
Posterior pillar (often associated with dislocation of hip and involves WB part of joint ® ORIF)
Transverse
Comminuted both column type (difficult to reduce and degenerative changes common)
4. Sacral / coccygeal fractures
Investigations:
Clinical examination
® associated injuries (bladder, urethra, spine, femurs etc)
signs hip ROM
obvious instability on compression/ springing
Destots sign- blood above inguinal lig or in scrotum
Roux's sign- decrease distance from gt troch to pubic tubercle
Earle's sign- tender swelling on PR
X-Rays
® standard AP
inlet view (tilt X-Ray beam 40o caudad) -shows post displacement
outlet view- ( 40o cranial beam)-shows superior migration or rotation
2 Judet views
CT scan and reconstructions ® plan surgical approach
Angiography and embolisation of bleeding vessels may be life saving
Treatment:
Resuscitation
fluid replacement
antishock garment
embolisation
direct surgical intervention
application of Ex Fix can reduce venous and bony bleeding signif
Provisional stabilisation
for fractures that increase pelvic volume ie open book (B1) or vertical shear (C3)
apply ex fix or pelvic clamp percutaneously in emerg room
Ex fix- 2 pins placed percut in Ileum- 1 at ASIS, 1 at iliac tubercle, at ~ 45 deg to each other- complate frame as anterior rectangle
By Type
A
symptomatic, mobilisation
B1
Stage 1 no stabilisation
2+3 stabilise with Ex fix or ant plate
B2+3
most need no stabilisation
B3 - displaced bucket handle
if LLD less than 1.5 cm- accept
if LLD more than 1.5 cm or pelvic deformity excessive- reduction by ER of hemipelvis with pins in the iliac crest, maintained with anterior frame
C
Options
Ant frame+ skeletal traction (supracondylar femoral pin)
-safe
-indicated if - adequate reduction of post sacroiliac complex
when post injury a iliac fracture rather than an S-I dislocation or a sacral fracture
-disadvantages traction for 8-12 wks
ORIF
- risks: bleeding - loss of tamponade, coagulopathy
infection
wound necrosis esp in post wounds
nerve damage
-indication: inadequate reduction of post injury(esp SI disloc)
open post wound
in assoc with acetabular fracture
Indications for Ex Fix
Type
B1
definitive treatment of stage 2+3
B2+3
to aid and maintain reduction
C
to produce partial stability to decrease bleeding, decrease pain, aid nursing
If ORIF to be performed should be delayed until patient stable, all investigations completed and operation planned but should not exceed 7 days
Complications:
Non-union / malunion ® high incidence of nerve, bladder etc complications at revision surgery (high incidence in Malgaine type 90%, and usually symptomatic)
ORIF delayed more than 3/52 ® callus formation which would limit reduction accuracy
Infection increased incidence associated with open bowel injury ® drain wounds
6% incidence and increased with ilio-inguinal approach ® avoid operations in febrile patients ® use prophylactic antibiotics
Nerve palsy (usually peroneal component) of sciatic nerve in 11.2% (17.4% of posterior fractures)
Ectopic bone formation in ~ 20% ® indomethicin useful ? carcinogenic effect of radiation in young people
Thrombo-embolic problems in ® anticoagulate for 6 - 8 weeks after open operation
RAH 3500 units heparin tds starting at 72 hours post injury or surgery and adjusted according to APTT (aim for APTT 31-36) ® warfarinise after one week post injury or operation ® therapeutic range (INR 2 - 2.5)
About 1/3 of unstable fractures (13% overall) have an associated urethral injury ® retrograde urethrogram prior to IDC ® cystogram ® IVP if indicated
Bladder rupture usually extra-peritoneal and may ® vesico colic, vesical fistulas
Impotence evident in ~ 40%
Post traumatic ost
Classification (Tile)
Type A: Stable
A1
Fracture not involving the ring
avulsion fracture of ASIS,AIIS or ischium
fracture of iliac wing
A2
Stable minimally displaced ring fractures
Type B:
Rotationally unstable / Vertically stable
B1
Open book
B2
Lateral compression (ipsilateral post and ant fractures)
Stage
separation of the symphysis less than 2.5 cm
-implies no post lesion
separation of symphysis more than 2.5 cm, unilat
more than 2.5 cm, bilat
-implies disruption of sacrospinous + ant sacroiliac ligs
B3
Lateral compression (contra-lateral post and ant fractures= bucket handle)
- the rotation of the bucket handle can cause gross pelvic deformity or significant LLD
External fixation ® definitive treatment, to aid or maintain reduction
Type C:
Rotationally and vertically unstable
C1: Unilateral
C2: Bilateral
C3: Associated with acetabular fractures
External fixation ® partial stability ® reduce bleeding, relieve pain and aid in nursing the patient
Posterior stabilisation may also be required
ref : Tile " pelvic ring fractures :should they be fixed" JBJS 70B:1-12, 1988
Classification (Apley)
1. Avulsions:
Due to violent muscle action
Sartorius from ASIS
Rectus femoris from AIIS
Adductor longus from pubis
Hamstrings form ischial tuberosity
Treatment ® rest and reassurance
2. Ring fractures:
Stable fractures ® symptomatic treatment
Disruption of posterior structures ® 4 - 6 weeks RIB
Unstable fractures;
Four poster
Open book
Malgaine type
Direct fractures of the iliac wing ® bed rest
Stress fractures of the pubis / pubic rami are not uncommon in osteoporotic patients
3. Acetabular fractures:
Anterior pillar (not WB part of joint)
Posterior pillar (often associated with dislocation of hip and involves WB part of joint ® ORIF)
Transverse
Comminuted both column type (difficult to reduce and degenerative changes common)
4. Sacral / coccygeal fractures
Investigations:
Clinical examination
® associated injuries (bladder, urethra, spine, femurs etc)
signs hip ROM
obvious instability on compression/ springing
Destots sign- blood above inguinal lig or in scrotum
Roux's sign- decrease distance from gt troch to pubic tubercle
Earle's sign- tender swelling on PR
X-Rays
® standard AP
inlet view (tilt X-Ray beam 40o caudad) -shows post displacement
outlet view- ( 40o cranial beam)-shows superior migration or rotation
2 Judet views
CT scan and reconstructions ® plan surgical approach
Angiography and embolisation of bleeding vessels may be life saving
Treatment:
Resuscitation
fluid replacement
antishock garment
embolisation
direct surgical intervention
application of Ex Fix can reduce venous and bony bleeding signif
Provisional stabilisation
for fractures that increase pelvic volume ie open book (B1) or vertical shear (C3)
apply ex fix or pelvic clamp percutaneously in emerg room
Ex fix- 2 pins placed percut in Ileum- 1 at ASIS, 1 at iliac tubercle, at ~ 45 deg to each other- complate frame as anterior rectangle
By Type
A
symptomatic, mobilisation
B1
Stage 1 no stabilisation
2+3 stabilise with Ex fix or ant plate
B2+3
most need no stabilisation
B3 - displaced bucket handle
if LLD less than 1.5 cm- accept
if LLD more than 1.5 cm or pelvic deformity excessive- reduction by ER of hemipelvis with pins in the iliac crest, maintained with anterior frame
C
Options
Ant frame+ skeletal traction (supracondylar femoral pin)
-safe
-indicated if - adequate reduction of post sacroiliac complex
when post injury a iliac fracture rather than an S-I dislocation or a sacral fracture
-disadvantages traction for 8-12 wks
ORIF
- risks: bleeding - loss of tamponade, coagulopathy
infection
wound necrosis esp in post wounds
nerve damage
-indication: inadequate reduction of post injury(esp SI disloc)
open post wound
in assoc with acetabular fracture
Indications for Ex Fix
Type
B1
definitive treatment of stage 2+3
B2+3
to aid and maintain reduction
C
to produce partial stability to decrease bleeding, decrease pain, aid nursing
If ORIF to be performed should be delayed until patient stable, all investigations completed and operation planned but should not exceed 7 days
Complications:
Non-union / malunion ® high incidence of nerve, bladder etc complications at revision surgery (high incidence in Malgaine type 90%, and usually symptomatic)
ORIF delayed more than 3/52 ® callus formation which would limit reduction accuracy
Infection increased incidence associated with open bowel injury ® drain wounds
6% incidence and increased with ilio-inguinal approach ® avoid operations in febrile patients ® use prophylactic antibiotics
Nerve palsy (usually peroneal component) of sciatic nerve in 11.2% (17.4% of posterior fractures)
Ectopic bone formation in ~ 20% ® indomethicin useful ? carcinogenic effect of radiation in young people
Thrombo-embolic problems in ® anticoagulate for 6 - 8 weeks after open operation
RAH 3500 units heparin tds starting at 72 hours post injury or surgery and adjusted according to APTT (aim for APTT 31-36) ® warfarinise after one week post injury or operation ® therapeutic range (INR 2 - 2.5)
About 1/3 of unstable fractures (13% overall) have an associated urethral injury ® retrograde urethrogram prior to IDC ® cystogram ® IVP if indicated
Bladder rupture usually extra-peritoneal and may ® vesico colic, vesical fistulas
Impotence evident in ~ 40%
Post traumatic ost
Hand Fractures
Scaphoid Fractures
ref: Gelberman etal "Fractures and nonunions of the carpal Scaphoid"
JBJS 71A:1560-1565, 1989
Blood supply:
From the radial artery both the dorsal and palmar branches but only two direct vascular leashes are observed entering the scaphoid
The most important of these are the scaphoid branches of the dorsal carpal branch of the radial artery entering the bone though the foramina along its dorsal ridge supplying 70 - 80% of the bone including the entire proximal pole
A second vessel or group of vessels from the palmar and superficial palmar branches enter the scaphoid in the region of its tuberosity to perfuse the distal 20 - 30% of the bone
The dorsal approach to the scaphoid places these vessels entering the dorsal ridge at highest risk
Pathology:
Approximately 30% of fractures of the middle third and nearly 100% of those of the proximal fifth are associated with osteonecrosis of the proximal pole
Treatment:
ref: Gellman etal "Comparison of Short and Long Thumb Spica casts for nondisplaced fractures of the carpal Scaphoid" JBJS 71A: 354-357, 1989
A prospective randomised clinical trial demonstrated a statistically significant advantage for treatment with a long thumb spica cast
Should be splinted in slight flexion and ulna deviation
Unstable (displaced fractures) should be internally fixed
Prognosis:
Undisplaced fractures united in 8 - 12 weeks when treated in a long thumb spica cast
Fractures of the distal 1/3 can be expected to unite in 6 - 8 weeks
middle 1/3 in 8 - 12 weeks
proximal 1/3 in 12 - 23 weeks
Complications:
Scaphoid non union ® OA develops in the adjacent carpal joints in more than 90% of cases within 5 yrs
This will be associated with discomfort in the majority of cases
Non-union ® carpal instability ® degenerative arthritis
Treatment:
Russe BG - 92% union rate ( iliac crest BG placed from volar side) (Matti = graft from dorsum- not done as risk to blood supply)
BG with fixation either K-wires or Herbert Screw
Late OA - difficult to treat- options include
Autograft eg costochondral
Allograft
Implant: silicone not used due to synovitis, hence titanium
scaphoid excision combined with intercarpal fusion
total wrist fusion
Scaphoid Malunion
can get markedly flexed scaphoid with a humpback deformity
osteotomy has been described to correct this - potential risks are of AVN of prox fragment
Dislocation of the MCP Joint of the Thumb:
Blocks to reduction include
Collateral ligament
Volar plate displaced into the joint
FPB or FPL tendons
Osteochondral fractures
Head button-holed through anterior capsule
Proximal phalanx button-holed through the extensor tendon
ref: Gelberman etal "Fractures and nonunions of the carpal Scaphoid"
JBJS 71A:1560-1565, 1989
Blood supply:
From the radial artery both the dorsal and palmar branches but only two direct vascular leashes are observed entering the scaphoid
The most important of these are the scaphoid branches of the dorsal carpal branch of the radial artery entering the bone though the foramina along its dorsal ridge supplying 70 - 80% of the bone including the entire proximal pole
A second vessel or group of vessels from the palmar and superficial palmar branches enter the scaphoid in the region of its tuberosity to perfuse the distal 20 - 30% of the bone
The dorsal approach to the scaphoid places these vessels entering the dorsal ridge at highest risk
Pathology:
Approximately 30% of fractures of the middle third and nearly 100% of those of the proximal fifth are associated with osteonecrosis of the proximal pole
Treatment:
ref: Gellman etal "Comparison of Short and Long Thumb Spica casts for nondisplaced fractures of the carpal Scaphoid" JBJS 71A: 354-357, 1989
A prospective randomised clinical trial demonstrated a statistically significant advantage for treatment with a long thumb spica cast
Should be splinted in slight flexion and ulna deviation
Unstable (displaced fractures) should be internally fixed
Prognosis:
Undisplaced fractures united in 8 - 12 weeks when treated in a long thumb spica cast
Fractures of the distal 1/3 can be expected to unite in 6 - 8 weeks
middle 1/3 in 8 - 12 weeks
proximal 1/3 in 12 - 23 weeks
Complications:
Scaphoid non union ® OA develops in the adjacent carpal joints in more than 90% of cases within 5 yrs
This will be associated with discomfort in the majority of cases
Non-union ® carpal instability ® degenerative arthritis
Treatment:
Russe BG - 92% union rate ( iliac crest BG placed from volar side) (Matti = graft from dorsum- not done as risk to blood supply)
BG with fixation either K-wires or Herbert Screw
Late OA - difficult to treat- options include
Autograft eg costochondral
Allograft
Implant: silicone not used due to synovitis, hence titanium
scaphoid excision combined with intercarpal fusion
total wrist fusion
Scaphoid Malunion
can get markedly flexed scaphoid with a humpback deformity
osteotomy has been described to correct this - potential risks are of AVN of prox fragment
Dislocation of the MCP Joint of the Thumb:
Blocks to reduction include
Collateral ligament
Volar plate displaced into the joint
FPB or FPL tendons
Osteochondral fractures
Head button-holed through anterior capsule
Proximal phalanx button-holed through the extensor tendon
Forearm Fractures
classification
Types
undisplaced
displaced
avulsion
transverse + oblique
comminuted
fracture / dislocations
Treatment
If undisplaced ® immobilise elbow for 3 - 4 weeks in a sling
If displaced (disruption or extensor mechanism) ® TBW
TBW with double twist ® strongest method of internal fixation for these fractures however a dorsal plate (positioned in tension) is also effective
Complications
reduced ROM - up to 50% have some loss of ROM - only ~ 3% have functional loss from this
post traumatic OA- rare as is a non wght bearing jt
Nonunion - ~5%
If high demand pt - ORIF/ BG
If low demand pt - may not need to do anything. Can excise the olecranon fragment with very good results ( as long as the coronoid and ant soft tissues are intact to provide stability)
Radial Head Fractures
Usually due to a fall onto the outstretched hand and may be associated with dislocation of the elbow
Over half of radial head fractures are associated with other injuries about the elbow
Classification: (Mason)
ref: Mason, M.L. "Some observations on fractures of the head of the Radius With a Review of 100 cases" Br J Surg 42: 123-132, 1954
Types
Undisplaced
Marginal fracture with displacement
Comminuted fracture with whole head involvement
Fracture of the radial head associated with dislocation of the elbow
NB: Type IV not described by Mason
Note that Essex- Lopresti (ALRUD) lesions can coexist
XRays
AP/ lat views of the elbow usually sufficient
fat pad sign
if no fracture seen but fat pad sign present - Radiocapitellar views with the forearm in neutral rotation and the XRay tube angled 45 deg cephalad
Treatment
Children
Acceptable angulation of 30o in young children as ® remodels with growth (15o in older children ie more than 10) and can expect 10o correction
If greater angulation than 30o ® either;
Manipulation under GA
Open reduction if more than 45o and irreducible
Never ® radial head excision in the young as ® ulna overgrowth
Adults
Type
nonoperative - early motion as soon as comfortable
without Essex- Lopresti
without mechanical block as for type 1
with mechanical block excise or ORIF
with Essex- Lopresti ORIF if at all possible ie retain head
May need to pin radius + ulna
without Essex- Lopresti or dislocation excise
with Essex- Lopresti aim to retain the head if at all possible
may need to transfix the radius and ulna to prevent translation
if the ant band of the MCL is disrupted need to repair primarily
aim to retain the radial head if at all possible
Summary
if head is salvageable do so
if Essex- Lopresti - save head, or if excise pin radius and ulna for 4-6/52
if elbow unstable ie MCL torn - save head, repair ligament if excise or not
In adults operation indicated if
Angulation more than 30o Depression of articular surface of more than 3mm
Greater than 1/3 of radial head involved
Complications
Reduced motion
Radial head overgrowth
Premature physeal closure
Non union
Avascular necrosis of the radial head
Alteration in the carrying angle
Neuromuscular problems (ie ® valgus with ulna nerve problems)
Radio/ulna synostosis
Myositis ossificans
Prognosis
The results of initial conservative management of Mason II and III fractures are no different to early excision
Also the results of delayed excision of the radial head are satisfactory giving some justification for the initial closed treatment of these fractures with delayed excision of the radial head to be considered at a later date if needed as symptoms develop
Fractures of Radius and Ulna
Galleazi fracture
fracture of distal 1/3 of radius with dislocation of the distal radioulnar jt ( Galleazi - 1934)
Treatment
ORIF in adults
CR/POP in children
aim to reduce accurately to ensure DRUJ reduction
Monteggia fracture
fracture of proximal ulna with dislocation of the prox radius ( Monteggia - Milan, 1814 )
Classification
( Bado)
Type
ant dislocation of radial head
post or posterolat dislocation of the radial head
lat or anterolat dislocation of the radial head
ant dislocation of the radial head with fracture of both radius and ulna at the diaphysis
Treatment
ORIF in adults
CR/POP in children
aim to reduce ulna - this reduces the prox jt
Nightstick Fracture
fracture ulnar diaphysis alone from a direct blow
Treatment
undisplaced
AEPOP or functional brace stopping supination/ pronation
displaced
ORIF
Prognosis
union in ~ 10 wks
nonunion - rare
Fracture of Shaft of Radius Alone
rare
Treatment
undisplaced
AEPOP or functional brace stopping supination/ pronation
displaced
ORIF
Fracture of Both Bones of Forearm
Classification based on the location in the forearm (proximal, middle or distal 1/3)
Treatment
Children
CR/POP - note the deforming forces of muscles at different levels of fracture
ORIF if unable to obtain or maintain reduction
Can accept 1cm overriding as long as the bones are correctly aligned and rotated
Can accept up to 20o angulation at the fracture in the skeletally immature (ie less than 10 years) ® no significant loss of pronation or supination providing the rotation of the individual bones is correct
Correction of angulation has been reported up to 18o (Larsen, 1988) mainly due to change in the orientation of the epiphyseal plate and appositional bone formation and resorption If close to cessation of growth require an anatomical reduction
Types
undisplaced
displaced
avulsion
transverse + oblique
comminuted
fracture / dislocations
Treatment
If undisplaced ® immobilise elbow for 3 - 4 weeks in a sling
If displaced (disruption or extensor mechanism) ® TBW
TBW with double twist ® strongest method of internal fixation for these fractures however a dorsal plate (positioned in tension) is also effective
Complications
reduced ROM - up to 50% have some loss of ROM - only ~ 3% have functional loss from this
post traumatic OA- rare as is a non wght bearing jt
Nonunion - ~5%
If high demand pt - ORIF/ BG
If low demand pt - may not need to do anything. Can excise the olecranon fragment with very good results ( as long as the coronoid and ant soft tissues are intact to provide stability)
Radial Head Fractures
Usually due to a fall onto the outstretched hand and may be associated with dislocation of the elbow
Over half of radial head fractures are associated with other injuries about the elbow
Classification: (Mason)
ref: Mason, M.L. "Some observations on fractures of the head of the Radius With a Review of 100 cases" Br J Surg 42: 123-132, 1954
Types
Undisplaced
Marginal fracture with displacement
Comminuted fracture with whole head involvement
Fracture of the radial head associated with dislocation of the elbow
NB: Type IV not described by Mason
Note that Essex- Lopresti (ALRUD) lesions can coexist
XRays
AP/ lat views of the elbow usually sufficient
fat pad sign
if no fracture seen but fat pad sign present - Radiocapitellar views with the forearm in neutral rotation and the XRay tube angled 45 deg cephalad
Treatment
Children
Acceptable angulation of 30o in young children as ® remodels with growth (15o in older children ie more than 10) and can expect 10o correction
If greater angulation than 30o ® either;
Manipulation under GA
Open reduction if more than 45o and irreducible
Never ® radial head excision in the young as ® ulna overgrowth
Adults
Type
nonoperative - early motion as soon as comfortable
without Essex- Lopresti
without mechanical block as for type 1
with mechanical block excise or ORIF
with Essex- Lopresti ORIF if at all possible ie retain head
May need to pin radius + ulna
without Essex- Lopresti or dislocation excise
with Essex- Lopresti aim to retain the head if at all possible
may need to transfix the radius and ulna to prevent translation
if the ant band of the MCL is disrupted need to repair primarily
aim to retain the radial head if at all possible
Summary
if head is salvageable do so
if Essex- Lopresti - save head, or if excise pin radius and ulna for 4-6/52
if elbow unstable ie MCL torn - save head, repair ligament if excise or not
In adults operation indicated if
Angulation more than 30o Depression of articular surface of more than 3mm
Greater than 1/3 of radial head involved
Complications
Reduced motion
Radial head overgrowth
Premature physeal closure
Non union
Avascular necrosis of the radial head
Alteration in the carrying angle
Neuromuscular problems (ie ® valgus with ulna nerve problems)
Radio/ulna synostosis
Myositis ossificans
Prognosis
The results of initial conservative management of Mason II and III fractures are no different to early excision
Also the results of delayed excision of the radial head are satisfactory giving some justification for the initial closed treatment of these fractures with delayed excision of the radial head to be considered at a later date if needed as symptoms develop
Fractures of Radius and Ulna
Galleazi fracture
fracture of distal 1/3 of radius with dislocation of the distal radioulnar jt ( Galleazi - 1934)
Treatment
ORIF in adults
CR/POP in children
aim to reduce accurately to ensure DRUJ reduction
Monteggia fracture
fracture of proximal ulna with dislocation of the prox radius ( Monteggia - Milan, 1814 )
Classification
( Bado)
Type
ant dislocation of radial head
post or posterolat dislocation of the radial head
lat or anterolat dislocation of the radial head
ant dislocation of the radial head with fracture of both radius and ulna at the diaphysis
Treatment
ORIF in adults
CR/POP in children
aim to reduce ulna - this reduces the prox jt
Nightstick Fracture
fracture ulnar diaphysis alone from a direct blow
Treatment
undisplaced
AEPOP or functional brace stopping supination/ pronation
displaced
ORIF
Prognosis
union in ~ 10 wks
nonunion - rare
Fracture of Shaft of Radius Alone
rare
Treatment
undisplaced
AEPOP or functional brace stopping supination/ pronation
displaced
ORIF
Fracture of Both Bones of Forearm
Classification based on the location in the forearm (proximal, middle or distal 1/3)
Treatment
Children
CR/POP - note the deforming forces of muscles at different levels of fracture
ORIF if unable to obtain or maintain reduction
Can accept 1cm overriding as long as the bones are correctly aligned and rotated
Can accept up to 20o angulation at the fracture in the skeletally immature (ie less than 10 years) ® no significant loss of pronation or supination providing the rotation of the individual bones is correct
Correction of angulation has been reported up to 18o (Larsen, 1988) mainly due to change in the orientation of the epiphyseal plate and appositional bone formation and resorption If close to cessation of growth require an anatomical reduction
Foot and Ankle Fractures
Ankle
Eponymous Types
Maisonneuve
either a med malleolus fracture or deltoid lig tear with a high fibular fracture
Le Fort - Wagstaffe
avulsion fracture of anterior margin of distal fibula at insertion of anterior tibio-fibular lig
Tillaux-Chaput
avulsion fracture of anterior tibial margin by the anterior tibio- fibular lig
Volkmanns triangle
the postero lat malleolar fracture
Classification: (Weber/ AO)
Type A
Transverse avulsion fracture of the fibula at the level of the ankle joint or below
Medial malleolus may be intact or sheared, and may be an associated compression fracture of the tibial edge
The tibio-fibular ligament complex is always intact
A1 isolated fibular fracture
A2 with fracture of med malleolus
A3 with a posteromedial fracture
Type B
Spiral fracture of the distal fibula beginning at the level of the syndesmosis
Part of the tibio-fibular syndesmotic ligament may be involved but the ankle mortise is stable following reduction of the fracture
B1 isolated fibular fracture
B2 with a med lesion ( malleolus or ligament)
B3 with a med lesion and fracture of posterolat tibia
Type C
Fracture of the fibula anywhere between the syndesmosis and the head of the fibula
The tibio-fibular ligament complex is always disrupted and diastasis screws should be inserted if it remains unstable after fixation of the fracture (ankle in neutral position when inserted)
C1 diaphyseal fracture of fibula- simple
C2 diaphyseal fracture of fibula- complex
C3 proximal fracture of fibula
Investigation
XRay
AP/lat/mortise views
stress views
Tomograms
CT
If X-Rays show a displaced malleolar fracture there must be a ligament injury somewhere around the mortice
Ramsey and Hamilton (1976) showed that lateral displacement of the talus in the mortice of 1mm an average 42% loss of articular contact and congruency
Treatment
Nonoperative
Indications
for undisplaced or stable fractures
for displaced fractures when anatomical reduction can be obtained and maintained without repeated manipulation
when pt general condition does not permit
when operative treatment delayed
obtained by reversing the mechanism of injury
maintained by AKPOP for rotationally unstable injuries, 3- point molding, ankle at 90
Undisplaced or stable fractures can be managed in BKPOP, WB PRN
Operative
Indications
failure of CR
when CR requires forced, abnormal positioning of the foot
for displaced or unstable fractures that result in displacement of the talus or
widening of the mortise of more than 1-2 mm
Aims
restore fibular length
anatomical jt surface reconstruction
close mortise: anatomic reconstruction of the fibula usually restores the mortise and restores stability to the syndesmosis
Syndesmotic fixation if: tibiofibular diastasis +/- high fibular fracture
instability post ORIF of fibula
Diastasis screws should be tri-cortical and not lagged
remove prior to WB
posterior malleolus- fix if more than 25% of artic surface and displaced more than 2mm most reduce with the fibular reduction
No significant benefit has been identified in the generally accepted regime of delayed application of plaster until after a reasonable range of movement has been achieved.
A paper from Nottingham suggests that females over 50 have higher incidence of complications of operative treatment- however this is a retrospective review and their overall figures are not very impressive ( Beauchamp etal "displaced ankle fractures in patients over 50 yrs of age" JBJS 65B: 329-332, 1983).
Their recommendation must be viewed with a degree of caution . A prospective trial from Chicago suggests that ORIF gives a better result in pts who are more than 50 yo ( Phillips etal JBJS 67A: 67, 1985)
Complications
Bone
nonunion
most of the med malleolus treated with CR- due to interposed tissue
treat if symptomatic with ORIF + BG
malunion
Wound
skin necrosis marginal necrosis in ~ 3%
care in handling tissue etc- treat with dressings
Infection
less than 2%, treat infection, leave fixation until fracture healed
Arthritis
incidence with severity of injury
degen changes in 10% of anatomically fixed , 85% if not adequately reduced - changes apparent within 18 mths
ref: Klossner "Late results of operative and nonoperative treatment of severe ankle fractures" Acta Chir Scand Suppl. 293: 1-93, 1962
Prognosis
There is a reduction in the incidence of arthrosis in patients where an anatomical reduction has been achieved
ref: Phillips etal JBJS 67A: 67-78, 1985 Prospective trial shows higher total ankle scores in those that are operatively treated- especially so in those pts more than 50 yrs old
Tillaux Fractures
Avulsion fracture of the anterolat distal tibia at site of attachment of the anterior tibio-fibular lig
= SH3 fracture
Triplane Fractures
Combine a Tillaux fracture with a type 2 S-H fracture
May be two or three part and fixation may cross the physis in these injuries as they occur when closure of the physis is imminent
Growth arrest occurs in 14% of all ankle fractures in the skeletally immature and appearance may be delayed for up to six months therefore need to check growth at one year
Treatment
ORIF
Prognosis
Residual dis
Eponymous Types
Maisonneuve
either a med malleolus fracture or deltoid lig tear with a high fibular fracture
Le Fort - Wagstaffe
avulsion fracture of anterior margin of distal fibula at insertion of anterior tibio-fibular lig
Tillaux-Chaput
avulsion fracture of anterior tibial margin by the anterior tibio- fibular lig
Volkmanns triangle
the postero lat malleolar fracture
Classification: (Weber/ AO)
Type A
Transverse avulsion fracture of the fibula at the level of the ankle joint or below
Medial malleolus may be intact or sheared, and may be an associated compression fracture of the tibial edge
The tibio-fibular ligament complex is always intact
A1 isolated fibular fracture
A2 with fracture of med malleolus
A3 with a posteromedial fracture
Type B
Spiral fracture of the distal fibula beginning at the level of the syndesmosis
Part of the tibio-fibular syndesmotic ligament may be involved but the ankle mortise is stable following reduction of the fracture
B1 isolated fibular fracture
B2 with a med lesion ( malleolus or ligament)
B3 with a med lesion and fracture of posterolat tibia
Type C
Fracture of the fibula anywhere between the syndesmosis and the head of the fibula
The tibio-fibular ligament complex is always disrupted and diastasis screws should be inserted if it remains unstable after fixation of the fracture (ankle in neutral position when inserted)
C1 diaphyseal fracture of fibula- simple
C2 diaphyseal fracture of fibula- complex
C3 proximal fracture of fibula
Investigation
XRay
AP/lat/mortise views
stress views
Tomograms
CT
If X-Rays show a displaced malleolar fracture there must be a ligament injury somewhere around the mortice
Ramsey and Hamilton (1976) showed that lateral displacement of the talus in the mortice of 1mm an average 42% loss of articular contact and congruency
Treatment
Nonoperative
Indications
for undisplaced or stable fractures
for displaced fractures when anatomical reduction can be obtained and maintained without repeated manipulation
when pt general condition does not permit
when operative treatment delayed
obtained by reversing the mechanism of injury
maintained by AKPOP for rotationally unstable injuries, 3- point molding, ankle at 90
Undisplaced or stable fractures can be managed in BKPOP, WB PRN
Operative
Indications
failure of CR
when CR requires forced, abnormal positioning of the foot
for displaced or unstable fractures that result in displacement of the talus or
widening of the mortise of more than 1-2 mm
Aims
restore fibular length
anatomical jt surface reconstruction
close mortise: anatomic reconstruction of the fibula usually restores the mortise and restores stability to the syndesmosis
Syndesmotic fixation if: tibiofibular diastasis +/- high fibular fracture
instability post ORIF of fibula
Diastasis screws should be tri-cortical and not lagged
remove prior to WB
posterior malleolus- fix if more than 25% of artic surface and displaced more than 2mm most reduce with the fibular reduction
No significant benefit has been identified in the generally accepted regime of delayed application of plaster until after a reasonable range of movement has been achieved.
A paper from Nottingham suggests that females over 50 have higher incidence of complications of operative treatment- however this is a retrospective review and their overall figures are not very impressive ( Beauchamp etal "displaced ankle fractures in patients over 50 yrs of age" JBJS 65B: 329-332, 1983).
Their recommendation must be viewed with a degree of caution . A prospective trial from Chicago suggests that ORIF gives a better result in pts who are more than 50 yo ( Phillips etal JBJS 67A: 67, 1985)
Complications
Bone
nonunion
most of the med malleolus treated with CR- due to interposed tissue
treat if symptomatic with ORIF + BG
malunion
Wound
skin necrosis marginal necrosis in ~ 3%
care in handling tissue etc- treat with dressings
Infection
less than 2%, treat infection, leave fixation until fracture healed
Arthritis
incidence with severity of injury
degen changes in 10% of anatomically fixed , 85% if not adequately reduced - changes apparent within 18 mths
ref: Klossner "Late results of operative and nonoperative treatment of severe ankle fractures" Acta Chir Scand Suppl. 293: 1-93, 1962
Prognosis
There is a reduction in the incidence of arthrosis in patients where an anatomical reduction has been achieved
ref: Phillips etal JBJS 67A: 67-78, 1985 Prospective trial shows higher total ankle scores in those that are operatively treated- especially so in those pts more than 50 yrs old
Tillaux Fractures
Avulsion fracture of the anterolat distal tibia at site of attachment of the anterior tibio-fibular lig
= SH3 fracture
Triplane Fractures
Combine a Tillaux fracture with a type 2 S-H fracture
May be two or three part and fixation may cross the physis in these injuries as they occur when closure of the physis is imminent
Growth arrest occurs in 14% of all ankle fractures in the skeletally immature and appearance may be delayed for up to six months therefore need to check growth at one year
Treatment
ORIF
Prognosis
Residual dis
Femur Fractures
Intracapsular Fractures of the Proximal Femur
Blood supply to the head of the femur
ref: Crock " An atlas of the arterial supply of the head and neck of the femur in man"
CORR 152: 1727, 1980
Chung JBJS 58A: 961970, 1976
4 groups 1. Extracapsular arterial ring
= trochanteric anastomosis
major contributions posteriorly from the horizontal br of the med circumflex femoral , and, anteriorly from ascending br of the lat femoral circumflex artery
2. Ascending cervical branches
( = retinacular br's) arise from 1.
pass up beneath the synovial and capsular reflections in their passage they give branches to the metaphysis of the femoral neck
there is a free intramedullary anastomosis bw branches of the superior nuttrient artery system,br's of the extracapsular ring, br's of the ascending cervical branches, and the subsynovial ring
4 groups sup, inf, med, lat the lateral supplies most of the blood to femoral head
at the margin of the artic cartilage these vessels form a second ring the
3. Subsynovial intracapsular ring ( Chung)
( = circulus articuli vasculosis Hunter, 1743). This ring may be complete or incomplete (complete more often in males). From this ring epiphyseal branches arise that enter the femoral head
4. Artery of the lig teres
from the lat br of the obturator artery supplies small area about the fovea in the vast majority
Epidemiology
increased freq with
age
dementia
malignancy
chronic illness
decreased freq with
long term physical activity
supplemental Vit D3 and Cain elderly women
HRT
Classification
Garden R.S. " Reduction and Fixation of subcapital fracturesof the femur"
OCNA 5: 683712, 1984
Types
an incomplete or impacted fracture
a complete but undisplaced fracture
a complete partially displaced fracture
a completely displaced fracture
Eliasson etal "Displacement in femoral neck fractures"
Acta Orth Scand 59:359371, 1988
Displaced ( = Garden 1+2)
Undisplaced (= Garden 3+4)
Treatment
based on pt age and grade of fracture
Pt less than 65
and do not have a chronic illness, poor life expectancy ® ORIF
Pt bw 65 and 75
those with high functional demand ® ORIF
those with low demand , chronic illness® arthroplasty
Pt more than 75
arthroplasty
pts of any age with less than 1 yr life expectancy® hemiarthroplasty
pts less than 75 with a limited life expectancy of more than 1yr®bipolar
Internal fixation
Timing of treatment
reduction of a displaced fracture of the femoral neck improves blood supply to the femoral head reduction within 8 12 hrs minimises risk of AVN if reduce within 8 hrs risk of AVN in a displaced fracture is ~ 20%.
2448 hrs risk is ~ 40%
ref: Swiontkowski etal JBJS 66A: 837846, 1984
Closed Reduction
Leadbetter ( ref : JBJS 20:108113, 1938)
affected hip flexed to 90 deg in slight adduction, traction then applied, then the thigh is internally rotated , then while maintaining IR the thigh is abducted and brought down to level in extension
Open Reduction
indicated if CR fails
anterolat approach bw TFL + G medius, open capsule, disimpact and reduce
Method of fixation
3 cannulated screws
CHS not recommended as is too large an implant and if placed incorrectly can jeopardise blood supply
If CHS used use a derotation screw to control rotation
Arthroplasty
AMP for pts more than 70
THR for pts less than 70
Complications
AVN
undisplaced fracture ~ 10%
displaced fracture up to ~ 80% either partial or complete (variable reporting)
late segmental collapse occurs in
~ 10% undisplaced fracture
~ 30% displaced fracture
Failure of fixation
Nonunion
rare in undisplaced fracture
~ 30% in displaced fracture
treat with either a valgus osteotomy or an arthroplasty
DVT/PE
DVT ~ 40%
low dose warfarin in pts who justify risk of anticoagulation
Prognosis
ref: LuYao etal " Outcomes after displaced fractures of the femoral neck"
JBJS 76A: 1525, 1994
Metaanalysis of 116 papers
At 2 yrs after primary ORIF
nonunion in 33%
AVN in 16%
reoperation rate 2036% ( ie 2.5 times that for hemiarthroplasty)
At 2 yrs from hemiarthroplasty
dislocation 2%
reoperation rate 618%
At 2 yrs from THR
dislocation 11%
Intertrochanteric Fractures
classification
AO
proximal femur type
A1 pertrochanteric simple
A2 pertrochanteric multifragmentary
A3 intertrochanteric
Kyle, Gustilo and Premer JBJS 61A: 216221, 1979
type 1: stable undisplaced , no comminution
type 2: stable displaced , min comminuted. Reduction ®stable construct
type 3: unstable , large posteromed comminuted area
type 4: also have a subtrochanteric component
Treatment
Type 1,2,3: ORIF with CHS
Type 4: CHS if pyriformis fossa not intact, supplemental BG
2nd generation nail if pyriformis fossa intact
no advantage to use osteotomies if using a sliding screw device
ref : Hopkins , Nugent and Dimon "Medial displacement Osteotomy for unstable intertrochanteric fractures" CORR 245: 169172, 1989
Complications/ Prognosis
Mortality
~ 30% at 1 yr , after this the expected normal curve is followed
Infection
~1%
Nonunion
rare
Mechanical / technical failures
nail cutting out
pin penetration
fracture below implant seen esp in gamma nail
Subtrochanteric fractures
Classification
Type 1
High: fracture line extends into the lesser trochanter
Type 2
Low: lesser trochanter remain
Blood supply to the head of the femur
ref: Crock " An atlas of the arterial supply of the head and neck of the femur in man"
CORR 152: 1727, 1980
Chung JBJS 58A: 961970, 1976
4 groups 1. Extracapsular arterial ring
= trochanteric anastomosis
major contributions posteriorly from the horizontal br of the med circumflex femoral , and, anteriorly from ascending br of the lat femoral circumflex artery
2. Ascending cervical branches
( = retinacular br's) arise from 1.
pass up beneath the synovial and capsular reflections in their passage they give branches to the metaphysis of the femoral neck
there is a free intramedullary anastomosis bw branches of the superior nuttrient artery system,br's of the extracapsular ring, br's of the ascending cervical branches, and the subsynovial ring
4 groups sup, inf, med, lat the lateral supplies most of the blood to femoral head
at the margin of the artic cartilage these vessels form a second ring the
3. Subsynovial intracapsular ring ( Chung)
( = circulus articuli vasculosis Hunter, 1743). This ring may be complete or incomplete (complete more often in males). From this ring epiphyseal branches arise that enter the femoral head
4. Artery of the lig teres
from the lat br of the obturator artery supplies small area about the fovea in the vast majority
Epidemiology
increased freq with
age
dementia
malignancy
chronic illness
decreased freq with
long term physical activity
supplemental Vit D3 and Cain elderly women
HRT
Classification
Garden R.S. " Reduction and Fixation of subcapital fracturesof the femur"
OCNA 5: 683712, 1984
Types
an incomplete or impacted fracture
a complete but undisplaced fracture
a complete partially displaced fracture
a completely displaced fracture
Eliasson etal "Displacement in femoral neck fractures"
Acta Orth Scand 59:359371, 1988
Displaced ( = Garden 1+2)
Undisplaced (= Garden 3+4)
Treatment
based on pt age and grade of fracture
Pt less than 65
and do not have a chronic illness, poor life expectancy ® ORIF
Pt bw 65 and 75
those with high functional demand ® ORIF
those with low demand , chronic illness® arthroplasty
Pt more than 75
arthroplasty
pts of any age with less than 1 yr life expectancy® hemiarthroplasty
pts less than 75 with a limited life expectancy of more than 1yr®bipolar
Internal fixation
Timing of treatment
reduction of a displaced fracture of the femoral neck improves blood supply to the femoral head reduction within 8 12 hrs minimises risk of AVN if reduce within 8 hrs risk of AVN in a displaced fracture is ~ 20%.
2448 hrs risk is ~ 40%
ref: Swiontkowski etal JBJS 66A: 837846, 1984
Closed Reduction
Leadbetter ( ref : JBJS 20:108113, 1938)
affected hip flexed to 90 deg in slight adduction, traction then applied, then the thigh is internally rotated , then while maintaining IR the thigh is abducted and brought down to level in extension
Open Reduction
indicated if CR fails
anterolat approach bw TFL + G medius, open capsule, disimpact and reduce
Method of fixation
3 cannulated screws
CHS not recommended as is too large an implant and if placed incorrectly can jeopardise blood supply
If CHS used use a derotation screw to control rotation
Arthroplasty
AMP for pts more than 70
THR for pts less than 70
Complications
AVN
undisplaced fracture ~ 10%
displaced fracture up to ~ 80% either partial or complete (variable reporting)
late segmental collapse occurs in
~ 10% undisplaced fracture
~ 30% displaced fracture
Failure of fixation
Nonunion
rare in undisplaced fracture
~ 30% in displaced fracture
treat with either a valgus osteotomy or an arthroplasty
DVT/PE
DVT ~ 40%
low dose warfarin in pts who justify risk of anticoagulation
Prognosis
ref: LuYao etal " Outcomes after displaced fractures of the femoral neck"
JBJS 76A: 1525, 1994
Metaanalysis of 116 papers
At 2 yrs after primary ORIF
nonunion in 33%
AVN in 16%
reoperation rate 2036% ( ie 2.5 times that for hemiarthroplasty)
At 2 yrs from hemiarthroplasty
dislocation 2%
reoperation rate 618%
At 2 yrs from THR
dislocation 11%
Intertrochanteric Fractures
classification
AO
proximal femur type
A1 pertrochanteric simple
A2 pertrochanteric multifragmentary
A3 intertrochanteric
Kyle, Gustilo and Premer JBJS 61A: 216221, 1979
type 1: stable undisplaced , no comminution
type 2: stable displaced , min comminuted. Reduction ®stable construct
type 3: unstable , large posteromed comminuted area
type 4: also have a subtrochanteric component
Treatment
Type 1,2,3: ORIF with CHS
Type 4: CHS if pyriformis fossa not intact, supplemental BG
2nd generation nail if pyriformis fossa intact
no advantage to use osteotomies if using a sliding screw device
ref : Hopkins , Nugent and Dimon "Medial displacement Osteotomy for unstable intertrochanteric fractures" CORR 245: 169172, 1989
Complications/ Prognosis
Mortality
~ 30% at 1 yr , after this the expected normal curve is followed
Infection
~1%
Nonunion
rare
Mechanical / technical failures
nail cutting out
pin penetration
fracture below implant seen esp in gamma nail
Subtrochanteric fractures
Classification
Type 1
High: fracture line extends into the lesser trochanter
Type 2
Low: lesser trochanter remain
Rheumatoid arthritis
Aetiology
At present unknown trigger or triggers stimulate or activate a disturbed immunologic response in a genetically susceptible individual.
Immune response genes congregated on the short arm of chromosome 6 in the segment called the major histo-compatibility complex. HLA antigens are the result of expression of genes in this segment.
Class I
Consist of 3 related types of molecules - HLA-A, -B, -C .Antigens are identified on all cells (except RBC + early embryonic tissue) ® identification of self, development of tolerance and strong graft rejection responses.
Class II
Code for molecules termed HLA -DR, -DQ and -DP. These are involved in antigen presentation to T- helper cells and are present
on B cells, macrophages and activated T or killer cells.
Aberrant induction of Class II antigen expression on cells other than those normally evident ® inflammation in some auto immune diseases.
Class III
Antigens are coded from a locus between Class I and II regions ® soluble proteins primarily involved in the complement cascade.
Rheumatic diseases associated with Class I antigens include arthropathies of the axial skeleton eg Ank Spond B27
Reiters B27
Psoriatic arthropathy B27 and B38
Class II antigens have an association with
eg Rheumatoid arthritis DR1 and DR4
Sjogrens' Syndrome DR2 and DR3
JCA
SLE DR2
The reason that more than one group of alleles can increase susceptibility to a disease is due to shared epitopes bw the molecules of each group.
eg the DR4 subgroup has 5 subtypes - of these only two - Dw4 and Dw14 promote susceptibility to RA - they share a common epitope in their beta chain
Rheumatoid arthritis is associated with HLA Dw4 locus and the HLA DR4 allotype in 60-80% of cases compared to only about 20-25% in the general population
Sero-negative patients account for 24% of those with the HLA DR4 allotype and sero-positive patients 55% indicating that they may be separate disease processes
The immune response triggers production of auto antibodies which form immune complexes and trigger synovial proliferation and inflammation resulting in the typical pathological features of Rheumatoid Arthritis.
Incidence
Affects 3% of the population
Approximately 300,000 RA sufferers in Australia
Usually presents in the 4th decade of life
M:F incidence 1:3
May affect any synovial joint and less commonly also cartilaginous joints and enthesies
Increased incidence in first degree relatives of RA patients
Pathogenesis
An at present unknown stimulus ® activation of immune system ® antibody / complement initiation of synovial inflammation and extra-articular manifestations in genetically susceptible individuals.
? viral (EB virus implicated), bacterial (component of bacterial cell wall may be stimulus), environmental, endogenous collagen or perhaps an emotional stimulus.
? stimulus ® formation of anti IgG Ab (Rh factor)
Activation of immune system ® release of proteolytic enzymes and digestion of tissue.
Immune reaction ® complement fixation and release of interleukin 1, phosphorylase A2, prostaglandin E2 and plasminogen ® degradation of matrix proteoglycan, induces synthesis of collagenase® chondrocyte death, cartilage breakdown augmenting the process of irreversible joint destruction.
It is postulated that cartilage is a necessary factor for the chronic process to begin and be maintained due to the fact that little recurrence is seen in artificial joint replacements.
Process blocked by early administration of cortisone ® proteoglycan synthesis is inhibited and existing proteoglycans are degraded.
Pathology
Begins as non specific inflammatory synovitis
® Non specific increase in capillaries
® Proliferation of synoviocytes
® Hypertrophy of synovium ® villi formation
® Lymphocytic and plasma cell infiltrate mainly peri vascular and formation of lymphocytic nodules
® Focal fibrinoid deposition
® Cellular necrosis
Highly vascular reduplicated synovium covers articular surface ® pannus formation
At the cartilage-pannus junction macrophages and fibroblasts are the predominant cell types
Presence of macrophages and collagenase markers within cells and the subsequent collagenolysis of the eroded bone matrix suggest that these cells may be responsible for a major portion of the bone erosion
These cells also secrete lysosomal enzymes such as proteases, cathepsin and elastase which are capable of degrading proteoglycan
RA artic cartilage specimens in a significant portion contain anti-collagen (Type II) antibodies
Pannus erodes the artic cartilage, Cartilage may fragment and ® intra-articular loose bodies
Subchondral bone is exposed and secondary osteoarthritis may result
There is associated local myositis
Rheumatoid Nodule
Central fibrinoid necrosis (fibrin, degraded collagen and cellular fragments) surrounded by a radially disposed palisades of local histiocytes and beyond that by inflammatory granulation tissue which is vascular and later becomes fibrotic. Peri vascular plasma cells and lymphocytes
Generally in Rh positive patients and usually implies more severe disease and vasculitis.
Seen on extensor surfaces, olecranon, lateral aspects of fingers, gluteal, Achilles, trochanters, ischial tuberosities, scapula, spine sacrum and occiput (if bedridden)
May become apparent before the actual onset of the arthritis
May persist indefinitely or regress
At present unknown trigger or triggers stimulate or activate a disturbed immunologic response in a genetically susceptible individual.
Immune response genes congregated on the short arm of chromosome 6 in the segment called the major histo-compatibility complex. HLA antigens are the result of expression of genes in this segment.
Class I
Consist of 3 related types of molecules - HLA-A, -B, -C .Antigens are identified on all cells (except RBC + early embryonic tissue) ® identification of self, development of tolerance and strong graft rejection responses.
Class II
Code for molecules termed HLA -DR, -DQ and -DP. These are involved in antigen presentation to T- helper cells and are present
on B cells, macrophages and activated T or killer cells.
Aberrant induction of Class II antigen expression on cells other than those normally evident ® inflammation in some auto immune diseases.
Class III
Antigens are coded from a locus between Class I and II regions ® soluble proteins primarily involved in the complement cascade.
Rheumatic diseases associated with Class I antigens include arthropathies of the axial skeleton eg Ank Spond B27
Reiters B27
Psoriatic arthropathy B27 and B38
Class II antigens have an association with
eg Rheumatoid arthritis DR1 and DR4
Sjogrens' Syndrome DR2 and DR3
JCA
SLE DR2
The reason that more than one group of alleles can increase susceptibility to a disease is due to shared epitopes bw the molecules of each group.
eg the DR4 subgroup has 5 subtypes - of these only two - Dw4 and Dw14 promote susceptibility to RA - they share a common epitope in their beta chain
Rheumatoid arthritis is associated with HLA Dw4 locus and the HLA DR4 allotype in 60-80% of cases compared to only about 20-25% in the general population
Sero-negative patients account for 24% of those with the HLA DR4 allotype and sero-positive patients 55% indicating that they may be separate disease processes
The immune response triggers production of auto antibodies which form immune complexes and trigger synovial proliferation and inflammation resulting in the typical pathological features of Rheumatoid Arthritis.
Incidence
Affects 3% of the population
Approximately 300,000 RA sufferers in Australia
Usually presents in the 4th decade of life
M:F incidence 1:3
May affect any synovial joint and less commonly also cartilaginous joints and enthesies
Increased incidence in first degree relatives of RA patients
Pathogenesis
An at present unknown stimulus ® activation of immune system ® antibody / complement initiation of synovial inflammation and extra-articular manifestations in genetically susceptible individuals.
? viral (EB virus implicated), bacterial (component of bacterial cell wall may be stimulus), environmental, endogenous collagen or perhaps an emotional stimulus.
? stimulus ® formation of anti IgG Ab (Rh factor)
Activation of immune system ® release of proteolytic enzymes and digestion of tissue.
Immune reaction ® complement fixation and release of interleukin 1, phosphorylase A2, prostaglandin E2 and plasminogen ® degradation of matrix proteoglycan, induces synthesis of collagenase® chondrocyte death, cartilage breakdown augmenting the process of irreversible joint destruction.
It is postulated that cartilage is a necessary factor for the chronic process to begin and be maintained due to the fact that little recurrence is seen in artificial joint replacements.
Process blocked by early administration of cortisone ® proteoglycan synthesis is inhibited and existing proteoglycans are degraded.
Pathology
Begins as non specific inflammatory synovitis
® Non specific increase in capillaries
® Proliferation of synoviocytes
® Hypertrophy of synovium ® villi formation
® Lymphocytic and plasma cell infiltrate mainly peri vascular and formation of lymphocytic nodules
® Focal fibrinoid deposition
® Cellular necrosis
Highly vascular reduplicated synovium covers articular surface ® pannus formation
At the cartilage-pannus junction macrophages and fibroblasts are the predominant cell types
Presence of macrophages and collagenase markers within cells and the subsequent collagenolysis of the eroded bone matrix suggest that these cells may be responsible for a major portion of the bone erosion
These cells also secrete lysosomal enzymes such as proteases, cathepsin and elastase which are capable of degrading proteoglycan
RA artic cartilage specimens in a significant portion contain anti-collagen (Type II) antibodies
Pannus erodes the artic cartilage, Cartilage may fragment and ® intra-articular loose bodies
Subchondral bone is exposed and secondary osteoarthritis may result
There is associated local myositis
Rheumatoid Nodule
Central fibrinoid necrosis (fibrin, degraded collagen and cellular fragments) surrounded by a radially disposed palisades of local histiocytes and beyond that by inflammatory granulation tissue which is vascular and later becomes fibrotic. Peri vascular plasma cells and lymphocytes
Generally in Rh positive patients and usually implies more severe disease and vasculitis.
Seen on extensor surfaces, olecranon, lateral aspects of fingers, gluteal, Achilles, trochanters, ischial tuberosities, scapula, spine sacrum and occiput (if bedridden)
May become apparent before the actual onset of the arthritis
May persist indefinitely or regress
Gout
Definition
Disorder of purine metabolism characterised by hyperuricaemia and recurrent attacks of acute synovitis due to urate crystal deposition
Associated with accumulation of articular, osseous, cartilaginous and soft tissue crystalline deposits (tophi)
Aetiology
Hyperuricaemia is the common denominator of the syndrome (all patients with gout have hyperuricaemia)
If levels increase above its solubility® crystal deposition
Hyperuricaemia is present in 2 - 18% of the population but only 5% of patients with hyperuricaemia® gout
Primary Hyperuricaemia
(Secondary to disordered uric acid metabolism)
Accounts for 95%
Inherited disorder with over production (20%) or under excretion (80%)
Classification based on 24 hour urine collection and urate excretion
Secondary Hyperuricaemia
Gout is a secondary feature of a number of genetic, or acquired processes and accounts for 5% of cases
Over-production:
Myelo-proliferative and lympho-proliferative disorders
(polycythemia, thrombocytopenia, myeloid metaplasia, leukaemias, lymphomas, paraprotinaemias, haemolytic anaemias, pernicious anaemia, infectious mononucleosis)
Cytotoxic and radiation therapy for malignancy
Psoriasis
Under excretion:
Renal disease
Drugs (thiazide diuretics and low dose salicylates)
Hyper and hypoparathyroidism
Myxoedema
Contributing Factors:
Diabetes
Hypertension and coronary heart disease
Excessive alcohol intake
High purine diets
Obesity
Low urine volume with normal renal function
90% of patients with gout have a disorder of uric acid excretion and drugs that alter renal tubular function can contribute to the occurrence of gout (eg diuretics, aspirin, ethanol)
Diuretics are the most common cause of secondary hyperuricaemia due to volume depletion and enhanced tubular resorption of urate
Increased risk of developing the disease with increasing age and serum urate concentration
Genetic studies suggest multi factorial inheritance
Incidence
20 - 30 / 100,000
Prevalence 0.13 - 0.37 % of population
Male : Female 20:1 (5% of cases are female)
Males usually more than 35 years, women usually more than 55 years
Gout is the most common form of inflammatory disease in men over 30 years of age
Rarely seen before the menopause in women
Clinically
Stages of Disease
Asymptomatic hyperuricaemia
Acute gouty arthritis
Inter-critical gout
Chronic tophacious gout
Acute Attack
Sudden attack of joint pain lasting several days
May follow trauma, surgery, drugs, exercise or alcohol
Commonly affects MTP joint of great toe (at least 50% of initial attack and 90% at some stage), also ankle and finger joints and the olecranon bursa
Joints feel hot and extremely tender
Hyperuricaemia is present at some stage
7% never have a second attack
60%® recurrent attack within one year
Negative birefringent crystals are seen in synovial fluid® diagnosis
X-Rays: Soft tissue swelling
Chronic Gout
Recurrent attacks® poly-articular gout, usually more severe, more prolonged and associated with fever
May be difficult to differentiate from other inflammatory arthropathies or infection
Joint erosions® chronic pain, stiffness and deformity
Tophi may appear around joints, olecranon and pinna of the ear
May ulcerate through the skin® discharge chalky material
Only a minority of patients develop visible tophi, permanent joint changes or chronic symptoms
Renal calculi may form and parenchymal renal disease occur secondary to crystal deposition with some renal dysfunction occurring in 90% of patients with gouty arthritis
In 10% gout is preceded by nephrolithiasis
Typically the first attack occurs during the night and tends to subside after 3 - 10 days
Tophi generally noted an average of 10 years after the first attack
X-Rays:
Symmetrical punched out cysts in extra-articular bone
Bony erosions either extra-articular or articular
Joint space is preserved until late in the disease
Pathology
Histopathology
Tophi® chronic foreign body granulation tissue surrounding urate crystals
Uric acid crystals deposited in synovium, tendons and tendon sheaths and articular cartilage
Results in activation of acute inflammation® cartilage degeneration and peri-articular cysts formation secondary to deposition of mono-sodium urate
Large cartilage and soft tissue tophi appear
Investigations
If excretion of uric acid is greater than 750mg per 24 hours suggests over production of urate
Measure 24 hour urate excretion after 1 week of a purine free diet® over production if more than 600mg and under excreter if less than 350mg per 24 hours
Synovial fluid® high cell count more than 90% neutrophils
Urate crystals usually remain in the synovium after the acute attack has settled
Compensated polarised light microscopy
With polarising filters and a first order red compensator monosodium urate crystals are 3-20mm in length needle shaped and strongly negatively birefringent (yellow in colour when the crystal axis is parallel to the compensator)
Calcium pyrophosphate crystals are short, rhomboidal and weakly positively birefringent (blue when the crystal axis is parallel to the compensator)
Differential Diagnosis
Infection
Reiters disease
Pseudo-gout (tends to affect large rather than small joints)
Rheumatoid arthritis
Arthritis mutilans
Treatment
Aim of therapy
Terminate the acute at
Disorder of purine metabolism characterised by hyperuricaemia and recurrent attacks of acute synovitis due to urate crystal deposition
Associated with accumulation of articular, osseous, cartilaginous and soft tissue crystalline deposits (tophi)
Aetiology
Hyperuricaemia is the common denominator of the syndrome (all patients with gout have hyperuricaemia)
If levels increase above its solubility® crystal deposition
Hyperuricaemia is present in 2 - 18% of the population but only 5% of patients with hyperuricaemia® gout
Primary Hyperuricaemia
(Secondary to disordered uric acid metabolism)
Accounts for 95%
Inherited disorder with over production (20%) or under excretion (80%)
Classification based on 24 hour urine collection and urate excretion
Secondary Hyperuricaemia
Gout is a secondary feature of a number of genetic, or acquired processes and accounts for 5% of cases
Over-production:
Myelo-proliferative and lympho-proliferative disorders
(polycythemia, thrombocytopenia, myeloid metaplasia, leukaemias, lymphomas, paraprotinaemias, haemolytic anaemias, pernicious anaemia, infectious mononucleosis)
Cytotoxic and radiation therapy for malignancy
Psoriasis
Under excretion:
Renal disease
Drugs (thiazide diuretics and low dose salicylates)
Hyper and hypoparathyroidism
Myxoedema
Contributing Factors:
Diabetes
Hypertension and coronary heart disease
Excessive alcohol intake
High purine diets
Obesity
Low urine volume with normal renal function
90% of patients with gout have a disorder of uric acid excretion and drugs that alter renal tubular function can contribute to the occurrence of gout (eg diuretics, aspirin, ethanol)
Diuretics are the most common cause of secondary hyperuricaemia due to volume depletion and enhanced tubular resorption of urate
Increased risk of developing the disease with increasing age and serum urate concentration
Genetic studies suggest multi factorial inheritance
Incidence
20 - 30 / 100,000
Prevalence 0.13 - 0.37 % of population
Male : Female 20:1 (5% of cases are female)
Males usually more than 35 years, women usually more than 55 years
Gout is the most common form of inflammatory disease in men over 30 years of age
Rarely seen before the menopause in women
Clinically
Stages of Disease
Asymptomatic hyperuricaemia
Acute gouty arthritis
Inter-critical gout
Chronic tophacious gout
Acute Attack
Sudden attack of joint pain lasting several days
May follow trauma, surgery, drugs, exercise or alcohol
Commonly affects MTP joint of great toe (at least 50% of initial attack and 90% at some stage), also ankle and finger joints and the olecranon bursa
Joints feel hot and extremely tender
Hyperuricaemia is present at some stage
7% never have a second attack
60%® recurrent attack within one year
Negative birefringent crystals are seen in synovial fluid® diagnosis
X-Rays: Soft tissue swelling
Chronic Gout
Recurrent attacks® poly-articular gout, usually more severe, more prolonged and associated with fever
May be difficult to differentiate from other inflammatory arthropathies or infection
Joint erosions® chronic pain, stiffness and deformity
Tophi may appear around joints, olecranon and pinna of the ear
May ulcerate through the skin® discharge chalky material
Only a minority of patients develop visible tophi, permanent joint changes or chronic symptoms
Renal calculi may form and parenchymal renal disease occur secondary to crystal deposition with some renal dysfunction occurring in 90% of patients with gouty arthritis
In 10% gout is preceded by nephrolithiasis
Typically the first attack occurs during the night and tends to subside after 3 - 10 days
Tophi generally noted an average of 10 years after the first attack
X-Rays:
Symmetrical punched out cysts in extra-articular bone
Bony erosions either extra-articular or articular
Joint space is preserved until late in the disease
Pathology
Histopathology
Tophi® chronic foreign body granulation tissue surrounding urate crystals
Uric acid crystals deposited in synovium, tendons and tendon sheaths and articular cartilage
Results in activation of acute inflammation® cartilage degeneration and peri-articular cysts formation secondary to deposition of mono-sodium urate
Large cartilage and soft tissue tophi appear
Investigations
If excretion of uric acid is greater than 750mg per 24 hours suggests over production of urate
Measure 24 hour urate excretion after 1 week of a purine free diet® over production if more than 600mg and under excreter if less than 350mg per 24 hours
Synovial fluid® high cell count more than 90% neutrophils
Urate crystals usually remain in the synovium after the acute attack has settled
Compensated polarised light microscopy
With polarising filters and a first order red compensator monosodium urate crystals are 3-20mm in length needle shaped and strongly negatively birefringent (yellow in colour when the crystal axis is parallel to the compensator)
Calcium pyrophosphate crystals are short, rhomboidal and weakly positively birefringent (blue when the crystal axis is parallel to the compensator)
Differential Diagnosis
Infection
Reiters disease
Pseudo-gout (tends to affect large rather than small joints)
Rheumatoid arthritis
Arthritis mutilans
Treatment
Aim of therapy
Terminate the acute at
Osteoarthritis
Definition
A degenerative joint disorder in which there is progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis.
Aetiology
Still obscure
Increased frequency with age but not an expression of senescence
Progression of cartilage lesions probable requires stiffened subchondral bone
Cartilage aging ® splitting and flaking of the surface and decreased cellularity, decreased proteoglycan ground substance and loss of elasticity with a decrease in breaking strength
Mechanical changes in subchondral bone ® stiffer and transmits more load to the cartilage
May be biological change secondary to a disturbance in lubrication of the joint and hence nutrition of cartilage
Two forms of degeneration:
Limited cartilage loss seen mainly away from load bearing areas and probably due to wear and tear.
Progressive cartilage destruction always maximal in the major load bearing area and associated with symptomatic OA
Hereditary aspects of OA:
Joint congruity, CSH / CDH / DDH, Perthes, SFCE
Gait and posture
Joint / ligament laxity
Pagets, inflammatory arthropathies
Incidence
People > 60 years old ® moderate to severe OA in 8%
25% of females and 16% of males have symptomatic OA
80% people > 80 years have radiological evidence of OA
Male = Female incidence but females more symptomatic
The hip, knee and spine most commonly affected
OA of the hip more common in males than females and often unilateral, 20% eventually ® involvement of the other side
Classification
Primary Osteoarthritis: (When no cause is obvious)
Poly-arthritis affecting finger joints, (chiefly distal, thumb (basal), big toe (MTP) and often also the knees and facet joint of the spine
Usually starts in the hands but many joints become involved
Stiffness and deformity may be marked but pain usually mild or in time becomes painless
Mainly affects post menopausal women and has a marked familial incidence
Heberdens nodular arthropathy ® distal IP joint of the hands only
Sometimes, particularly in men the DIP joint changes are absent but other joints symmetrically involved and spinal changes pronounced
Primary generalised OA is associated with increased incidence of CTS and tenosynovitis
The arthropathy of the individual joints has the same pathology as mono-articular OA
Differentiate spinal changes from DISH, and distal IP joint changes from psoriatic arthropathy and gout
Secondary Osteoarthritis: (When it follows a demonstrable abnormality)
Secondary OA estimated to account for 80% of osteoarthritis
Articular degeneration results from a disparity in the stress applied to articular cartilage and the ability of the cartilage to withstand that stress.
Solomon (1976); Aetiology of OA
Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of articular cartilage due to defective subchondral bone
Classification of cartilage degeneration: (Jackson)
Class 1: Softening of articular cartilage
Class 2: Fibrillation and fissuring of articular cartilage
Class 3: Partial thickness cartilage loss, clefts and chondral flaps
Class 4: Full thickness cartilage loss with bone exposed
Clinically
Usually history of previous injury or pathology evident
History of intermittent disability
Usually present with pain
May experience decreased pain as the disease ® decreased ROM
Often worse on rising from bed and at the end of the day, aggravated by activity
Exaggerated by extremes of movement
Early ® relieved by rest, later ® pain at rest
Source of pain Helal (1965)
Capsular; due to stretch at extremes of movement
Muscular: following effort
Venous congestion: ® rest pain?
Movement may be associated with crepitus
Joint effusion or osteophytes may be evident
Muscle wasting may also be a feature
Deformity may precede the development of OA, but may also result from secondary muscle imbalance, capsular contracture or joint instability.
In the hip abduction, extension and internal rotation are affected first
Hip pain referred to the knee due to the fact that the obturator nerve supplies both joints (the sciatic and femoral do as well)
X-Rays
Joint space narrowing
Sub-articular sclerosis
Bone cysts
Osteophytes
Bone density is either normal or increased
There may be evidence of other pathology eg, old trauma, congenital anomalies, RA, chondrocalcinosis etc
Rapid and severe joint changes may occur, especially in patients taking analgesics and NSAIDs
Pathology
Capsule
Capsular ligament is supplied by both myelinated and non-myelinated nerves, the synovial layer by only non-myelinated nerves
Synovium
Secrete Hyaluronate (+ lubricin)
Two cell types
Type A: phagocytosis
Type B: secretory role
Complete absence of a basement membrane
Regulates movement of solutes, electrolytes and proteins
Synovial fluid a dialyslate of plasma and hyaluronate but has less high molecular weight proteins (eg fibrinogen) and more low molecular weight protein (eg albumin)
Cartilage is connective tissue derived from the mesenchyme
Articular cartilage is avascular, aneural and alymphatic, and a small number of chondrocytes are surrounded by a large quantity of extracellular matrix
The structure of this intercellular matrix determines the type of cartilage
Normal cartil
A degenerative joint disorder in which there is progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis.
Aetiology
Still obscure
Increased frequency with age but not an expression of senescence
Progression of cartilage lesions probable requires stiffened subchondral bone
Cartilage aging ® splitting and flaking of the surface and decreased cellularity, decreased proteoglycan ground substance and loss of elasticity with a decrease in breaking strength
Mechanical changes in subchondral bone ® stiffer and transmits more load to the cartilage
May be biological change secondary to a disturbance in lubrication of the joint and hence nutrition of cartilage
Two forms of degeneration:
Limited cartilage loss seen mainly away from load bearing areas and probably due to wear and tear.
Progressive cartilage destruction always maximal in the major load bearing area and associated with symptomatic OA
Hereditary aspects of OA:
Joint congruity, CSH / CDH / DDH, Perthes, SFCE
Gait and posture
Joint / ligament laxity
Pagets, inflammatory arthropathies
Incidence
People > 60 years old ® moderate to severe OA in 8%
25% of females and 16% of males have symptomatic OA
80% people > 80 years have radiological evidence of OA
Male = Female incidence but females more symptomatic
The hip, knee and spine most commonly affected
OA of the hip more common in males than females and often unilateral, 20% eventually ® involvement of the other side
Classification
Primary Osteoarthritis: (When no cause is obvious)
Poly-arthritis affecting finger joints, (chiefly distal, thumb (basal), big toe (MTP) and often also the knees and facet joint of the spine
Usually starts in the hands but many joints become involved
Stiffness and deformity may be marked but pain usually mild or in time becomes painless
Mainly affects post menopausal women and has a marked familial incidence
Heberdens nodular arthropathy ® distal IP joint of the hands only
Sometimes, particularly in men the DIP joint changes are absent but other joints symmetrically involved and spinal changes pronounced
Primary generalised OA is associated with increased incidence of CTS and tenosynovitis
The arthropathy of the individual joints has the same pathology as mono-articular OA
Differentiate spinal changes from DISH, and distal IP joint changes from psoriatic arthropathy and gout
Secondary Osteoarthritis: (When it follows a demonstrable abnormality)
Secondary OA estimated to account for 80% of osteoarthritis
Articular degeneration results from a disparity in the stress applied to articular cartilage and the ability of the cartilage to withstand that stress.
Solomon (1976); Aetiology of OA
Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of articular cartilage due to defective subchondral bone
Classification of cartilage degeneration: (Jackson)
Class 1: Softening of articular cartilage
Class 2: Fibrillation and fissuring of articular cartilage
Class 3: Partial thickness cartilage loss, clefts and chondral flaps
Class 4: Full thickness cartilage loss with bone exposed
Clinically
Usually history of previous injury or pathology evident
History of intermittent disability
Usually present with pain
May experience decreased pain as the disease ® decreased ROM
Often worse on rising from bed and at the end of the day, aggravated by activity
Exaggerated by extremes of movement
Early ® relieved by rest, later ® pain at rest
Source of pain Helal (1965)
Capsular; due to stretch at extremes of movement
Muscular: following effort
Venous congestion: ® rest pain?
Movement may be associated with crepitus
Joint effusion or osteophytes may be evident
Muscle wasting may also be a feature
Deformity may precede the development of OA, but may also result from secondary muscle imbalance, capsular contracture or joint instability.
In the hip abduction, extension and internal rotation are affected first
Hip pain referred to the knee due to the fact that the obturator nerve supplies both joints (the sciatic and femoral do as well)
X-Rays
Joint space narrowing
Sub-articular sclerosis
Bone cysts
Osteophytes
Bone density is either normal or increased
There may be evidence of other pathology eg, old trauma, congenital anomalies, RA, chondrocalcinosis etc
Rapid and severe joint changes may occur, especially in patients taking analgesics and NSAIDs
Pathology
Capsule
Capsular ligament is supplied by both myelinated and non-myelinated nerves, the synovial layer by only non-myelinated nerves
Synovium
Secrete Hyaluronate (+ lubricin)
Two cell types
Type A: phagocytosis
Type B: secretory role
Complete absence of a basement membrane
Regulates movement of solutes, electrolytes and proteins
Synovial fluid a dialyslate of plasma and hyaluronate but has less high molecular weight proteins (eg fibrinogen) and more low molecular weight protein (eg albumin)
Cartilage is connective tissue derived from the mesenchyme
Articular cartilage is avascular, aneural and alymphatic, and a small number of chondrocytes are surrounded by a large quantity of extracellular matrix
The structure of this intercellular matrix determines the type of cartilage
Normal cartil
Monday, November 1, 2010
Diabetes mellitus
Types
Type1 -insulin sensitive
Type2 -ins. Resistant
MODY- maturity onset diabetis of young
criteria for diagnosis
@ symptoms plus random alone sugar >200 mg% or fasting >125%
@ after 2hr GTT >200mg %
Pathogenesis
# Type1-
1 autoimmune factor -
insulitis
2 immunological marker- islet cell Ab
3 Enviromental- coxsackie n rubella
# Type 2
1 impaired Secretion, peripheral insulin resistance
excessive hepatic glucose production
# MODY
homozygous mutation of glucokinase
Complication
#acute
diabetic ketoacidosis n hyperglycemic hyperosmol. Coma
# chronic
@ microvascular
retinopathy , macular edema, sensory n motor mono or polyneuropathy, nephropathy
@ macrovascular
coronary art dis. , PVD, cerebral vascular dis,
@ other
GI: diarhea , gastroparesis
genitourinary: uropathy n sexual dysfunctn
dermatological , infection, cataract glaucoma
C/F
Type 1
age < 40, duration- days 2 wks, normal 2 wasted body habitus, polyuria, polydysia, polyphagia, plasma insulin low Type 2 age>40, mths 2 yrs duration, obese, diabetic ketoacidosis doesnt develop, norm or increased pl insulin.
Benedicts test
If reducing sugar in glucose it gives quantitive rslts
light green- 0.1 - 0.5 g%
green - 0.5-1 g%
yellow -1-2g%
red - >2g%
Treatment
Drugs
1 sulphonylurea
@ insulin secretogogues
@ chlorpropamide 100- 500 mg, tolbutamide 500-3000mg, glibenclamide n glipizide 2.5-20mg
@ side eff. Hypoglycemia , wt gain
2 meglitinide
@ repaglinide, nateglinide, meglitinide-o.5-16 mg/day
3 Biguanide
@ metformin - reduce hepatic glucose prod. N improve periphera glu. utilisation.
@ doesnt produce wt gain so useful in obese pts wth type DM
@ started at dose of 500mg twicd day n gradually increased 2 max of 1g tds
@ side eff. acidosis, anorexia, diarhea, metallic taste.
4 alpha glucosidase inhibitors
@ acarbose n miglitol- 25mg
@ inhibits alpha glucosidase enzyme leads to poor absorption of carbohydrates thereby causing reduced rise in post prandial glucose
5 thiazolidinediones
@ rosiglitazone 2-8 mg OD or pioglitazone 15-25 mg/day
@ the bind 2 peroxisome proliferator activated receptor that regulates transcription of genes involved in lipid metabolism n insulin action. This promotes adipocyte diff. N reduce ins resistnce
@ side eff. Wt gain
6. other
@glucagon like peptide 1 analogues
@ dipeptidyl peptidase IV inhibitor - vildagliptin n sitagliptin
#Insulin was discovered in 1921 .
#until 1980 it was obtained by extraction & purification from pancreas of cow & pig.
#the use of recombinant DNA technology has enabled large scale production of human insulin.
#it has transformed the management of type 1 DM.
CLASSIFICATION.
It is classified as per duration of action.(all figures in hours)
1. Rapid acting (insulin analogues- lispro, aspart, glulisine)
onset= <0.5
peak= 0.5 to 2.5
duration =3 to 4.5
2. Short acting(soluble regular)
o=0.5 to 1
p=1 to 4
d=4 to 8
3. Intermediate acting (isophane, lente)
o=1 to 3
p=3 to 8
d=7 to 14
4. Long acting(bovine ultralente)
o=2 to 4
p=6 to 12
d=12 to 30
5. Long acting(insulin analogue- glargine, detemir)
o=1 to 2
p=none
d=18 to 24
INSULIN DELIVERY.
1.It is injected s.c. into d anterior abdominal wall, upper arms, outer thigh & buttocks.
2.The rate of absorption of insulin is influenced by many factors other than the insulin formulation including the site, depth and volume of injection, skin temp, local massage & exercise.
3. Absorption is delayed from areas of lipohypertrophy at injection sites, which results from the local trophic action of insulin. So repeated injections at d same sites should be avoided.
4. Short acting has to be injected atleast 30min b4 a meal..
5. Fast acting ones can be administered immediately b4 food or even after meals.
6. Once in blood it has a half life of few minutes.
7. It is removed mainly by liver & also the kidneys.
INSULIN REGIMEN.
1. The choice of regimen depends on d desired degree of glycemic control, patient's lifestyle & ability to adjust the insulin dose.
2. Most ppl require 2 or more injections of insulin daily.
3. Once daily regimen is rarely sufficient.
4. Twice daily administration of a short acting and intermediate acting insulin given in combination b4 breakfast & evening meal is d simplest regimen & is still commonly used.
5. Individual requirement vary considerably act usually 2/3rd of total daily dose is given in morning in ratio of 1:2, short:intermediate acting insulin.
6. The remaining third is given in d evening.
SIDE EFFECTS.
1. Hypoglycemia
2. Weight gain
3. Peripheral edema
4. Insulin antibodies
5. Local allergy
6. Lipodystrophy @ injection site
DAWN PHENOMENON.
It is fasting hypoglycemia caused by release of counter regulatory hormones during d night as part of d normal circadian rhythm which increase insulin requirement b4 wakening.
Type1 -insulin sensitive
Type2 -ins. Resistant
MODY- maturity onset diabetis of young
criteria for diagnosis
@ symptoms plus random alone sugar >200 mg% or fasting >125%
@ after 2hr GTT >200mg %
Pathogenesis
# Type1-
1 autoimmune factor -
insulitis
2 immunological marker- islet cell Ab
3 Enviromental- coxsackie n rubella
# Type 2
1 impaired Secretion, peripheral insulin resistance
excessive hepatic glucose production
# MODY
homozygous mutation of glucokinase
Complication
#acute
diabetic ketoacidosis n hyperglycemic hyperosmol. Coma
# chronic
@ microvascular
retinopathy , macular edema, sensory n motor mono or polyneuropathy, nephropathy
@ macrovascular
coronary art dis. , PVD, cerebral vascular dis,
@ other
GI: diarhea , gastroparesis
genitourinary: uropathy n sexual dysfunctn
dermatological , infection, cataract glaucoma
C/F
Type 1
age < 40, duration- days 2 wks, normal 2 wasted body habitus, polyuria, polydysia, polyphagia, plasma insulin low Type 2 age>40, mths 2 yrs duration, obese, diabetic ketoacidosis doesnt develop, norm or increased pl insulin.
Benedicts test
If reducing sugar in glucose it gives quantitive rslts
light green- 0.1 - 0.5 g%
green - 0.5-1 g%
yellow -1-2g%
red - >2g%
Treatment
Drugs
1 sulphonylurea
@ insulin secretogogues
@ chlorpropamide 100- 500 mg, tolbutamide 500-3000mg, glibenclamide n glipizide 2.5-20mg
@ side eff. Hypoglycemia , wt gain
2 meglitinide
@ repaglinide, nateglinide, meglitinide-o.5-16 mg/day
3 Biguanide
@ metformin - reduce hepatic glucose prod. N improve periphera glu. utilisation.
@ doesnt produce wt gain so useful in obese pts wth type DM
@ started at dose of 500mg twicd day n gradually increased 2 max of 1g tds
@ side eff. acidosis, anorexia, diarhea, metallic taste.
4 alpha glucosidase inhibitors
@ acarbose n miglitol- 25mg
@ inhibits alpha glucosidase enzyme leads to poor absorption of carbohydrates thereby causing reduced rise in post prandial glucose
5 thiazolidinediones
@ rosiglitazone 2-8 mg OD or pioglitazone 15-25 mg/day
@ the bind 2 peroxisome proliferator activated receptor that regulates transcription of genes involved in lipid metabolism n insulin action. This promotes adipocyte diff. N reduce ins resistnce
@ side eff. Wt gain
6. other
@glucagon like peptide 1 analogues
@ dipeptidyl peptidase IV inhibitor - vildagliptin n sitagliptin
#Insulin was discovered in 1921 .
#until 1980 it was obtained by extraction & purification from pancreas of cow & pig.
#the use of recombinant DNA technology has enabled large scale production of human insulin.
#it has transformed the management of type 1 DM.
CLASSIFICATION.
It is classified as per duration of action.(all figures in hours)
1. Rapid acting (insulin analogues- lispro, aspart, glulisine)
onset= <0.5
peak= 0.5 to 2.5
duration =3 to 4.5
2. Short acting(soluble regular)
o=0.5 to 1
p=1 to 4
d=4 to 8
3. Intermediate acting (isophane, lente)
o=1 to 3
p=3 to 8
d=7 to 14
4. Long acting(bovine ultralente)
o=2 to 4
p=6 to 12
d=12 to 30
5. Long acting(insulin analogue- glargine, detemir)
o=1 to 2
p=none
d=18 to 24
INSULIN DELIVERY.
1.It is injected s.c. into d anterior abdominal wall, upper arms, outer thigh & buttocks.
2.The rate of absorption of insulin is influenced by many factors other than the insulin formulation including the site, depth and volume of injection, skin temp, local massage & exercise.
3. Absorption is delayed from areas of lipohypertrophy at injection sites, which results from the local trophic action of insulin. So repeated injections at d same sites should be avoided.
4. Short acting has to be injected atleast 30min b4 a meal..
5. Fast acting ones can be administered immediately b4 food or even after meals.
6. Once in blood it has a half life of few minutes.
7. It is removed mainly by liver & also the kidneys.
INSULIN REGIMEN.
1. The choice of regimen depends on d desired degree of glycemic control, patient's lifestyle & ability to adjust the insulin dose.
2. Most ppl require 2 or more injections of insulin daily.
3. Once daily regimen is rarely sufficient.
4. Twice daily administration of a short acting and intermediate acting insulin given in combination b4 breakfast & evening meal is d simplest regimen & is still commonly used.
5. Individual requirement vary considerably act usually 2/3rd of total daily dose is given in morning in ratio of 1:2, short:intermediate acting insulin.
6. The remaining third is given in d evening.
SIDE EFFECTS.
1. Hypoglycemia
2. Weight gain
3. Peripheral edema
4. Insulin antibodies
5. Local allergy
6. Lipodystrophy @ injection site
DAWN PHENOMENON.
It is fasting hypoglycemia caused by release of counter regulatory hormones during d night as part of d normal circadian rhythm which increase insulin requirement b4 wakening.
Amenorrhoea
,Amenorrhoea : absence of menstruatino two types Primary secondary
primary amenorrhoea :failure of onset of menstruatino beyond age of 16 years regardless of development of secondary sexual character .
Classification it is made on basis of serum FSHlevel
! Hyper gonadotropic 2 eu gonadotropic 3 hypo gonadotropic
etiology: 1delayed puberty 2 cerebral stress emotional disturbane infection trauma tumor 3 hypothalamus kallmans syndrome vigorous exercise weight loss 4 pituitary gland empty sella turcica cushings syndrome frohlich syndrome 5 ovary turner syndrome savage syndrome PCOD genital tract absent uterus refractory endometrium obstruction in lower genital tract 7 chromosomal 8 drugs anti hyper tensive 9 nutrition
MANAGEMEnt A hyper gonadotropic : there is gonadal failure or dys genesis FSH > 4o miu/ml chromosomal 45 xo 1 GONADECTOMY in pt of testicular feminizing syndrome 2 OOCYTE donation 3 cyclic oestrogen and progesterone
EU gonado tropic : FSH normal testicular feminizing syndrome with 46 xy 1 prophylactic GONADECtomy 2 oestrogen therapy 3 vagino plasty 4 creation of functional vagina for coitus 5 simple cruciate incision of hymen
c hypo gonado tropic : FSH < 4O due to hypothalamic dys function pituitory dys fun 1 GnRH therapy
General therapy 1 HRT 2 nutrition 3 psychogenic therapy ,,
primary amenorrhoea :failure of onset of menstruatino beyond age of 16 years regardless of development of secondary sexual character .
Classification it is made on basis of serum FSHlevel
! Hyper gonadotropic 2 eu gonadotropic 3 hypo gonadotropic
etiology: 1delayed puberty 2 cerebral stress emotional disturbane infection trauma tumor 3 hypothalamus kallmans syndrome vigorous exercise weight loss 4 pituitary gland empty sella turcica cushings syndrome frohlich syndrome 5 ovary turner syndrome savage syndrome PCOD genital tract absent uterus refractory endometrium obstruction in lower genital tract 7 chromosomal 8 drugs anti hyper tensive 9 nutrition
MANAGEMEnt A hyper gonadotropic : there is gonadal failure or dys genesis FSH > 4o miu/ml chromosomal 45 xo 1 GONADECTOMY in pt of testicular feminizing syndrome 2 OOCYTE donation 3 cyclic oestrogen and progesterone
EU gonado tropic : FSH normal testicular feminizing syndrome with 46 xy 1 prophylactic GONADECtomy 2 oestrogen therapy 3 vagino plasty 4 creation of functional vagina for coitus 5 simple cruciate incision of hymen
c hypo gonado tropic : FSH < 4O due to hypothalamic dys function pituitory dys fun 1 GnRH therapy
General therapy 1 HRT 2 nutrition 3 psychogenic therapy ,,
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